Chapter 1

Diet and Disease
Diet and Disease

Nutrition for Gastrointestinal,
Musculoskeletal, Hepatobiliary,
Pancreatic, and Kidney Diseases
Katie Ferraro, MPH, RD, CDE
Diet and Disease: Nutrition for Gastrointestinal, Musculoskeletal, Hepatobiliary,

Pancreatic, and Kidney Diseases
Copyright Momentum Press, LLC, 2016
All rights reserved. No part of this publication may be reproduced, stored
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First published in 2016 by
Momentum Press, LLC
222 East 46th Street, New York, NY 10017
www.momentumpress.net
ISBN-13: 978-1-60650-921-0 (print)
ISBN-13: 978-1-60650-922-7 (e-book)
Momentum Press Nutrition and Dietetics Practice Collection
DOI: 10.5643/9781606509227
Cover and interior design by S4Carlisle Publishing Services Private Ltd.,
Chennai, India
First edition: 2016
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Printed in the United States of America.
Abstract
Let food be thy medicine and medicine be thy food.
Hippocrates
Can food really take the place of medicine? While modern medicine certainly has its place and does more than its fair share of good, there is no
denying that many of societys most perilous chronic diseases are exacerbated by poor diets. Whereas earlier infectious diseases used to cause the
most death, the impact of chronic diseases now far overshadows that of
infectious diseases. Diet plays a significant role in the development of a
number of types of chronic disease, such as heart disease, diabetes, and
certain types of cancer. This title explores the impact of dietary choices
on the prevention, management, and treatment of a number of medical
conditions and disease states including the gastrointestinal tract, musculoskeletal disorders, rheumatic disease, anemias, hepatobiliary, gallbladder, pancreatic, and kidney diseases. The topics of nutrition and cardiovascular disease, diabetes and metabolic stress, critical illness, cancer and
HIV/AIDS are covered in the subsequent title Diet and Disease I.
Keywords
Medical nutrition therapy, diet and disease, nutrition care process, diet
therapy, gastrointestinal disorders, musculoskeletal diseases, osteoporosis,
kidney disease diet, liver disease diet
Contents
List of Tables ........................................................................................ ix
Chapter 1
Chapter 2
Chapter 3
Nutrition and Gastrointestinal Disorders ..........................1

Musculoskeletal Disorders, Rheumatic
Disease, and Anemias .....................................................53
Hepatobiliary, Gallbladder,
Pancreatic, and Kidney Diseases .....................................91
Index.................................................................................................111
List of Tables
Table 1.1
Primary sites of nutrient absorption ..................................5
Table 1.2
Lipoproteins, their content, roles in the body and

health implications ...........................................................7
Table 1.3
Xerostomia treatment techniques and

products to avoid (AND, 2015)........................................8
Table 1.4
Nutritional consequences of untreated

dysphagia (AND, 2015a) ................................................10
Table 1.5
The National Dysphagia Diet food considerations

(McCallum 2003), (McCullough, Pelletier and Steele
2003) .............................................................................11
Table 1.6
National Dysphagia Diet liquid consistencies

(AND, 2015a) ................................................................12
Table 1.7
Nutrition interventions and goals in patients with

GERD (AND, 2015b)....................................................14
Table 1.8
Diet therapy for patients with GERD (AND, 2015b),

(Hasler 2015) ..................................................................14
Table 1.9
Factors that exacerbate peptic ulcer disease

(AND, 2015c) ................................................................16
Table 1.10 Foods not recommended for people with peptic

ulcer disease (AND, 2015c) ............................................17
Table 1.11 Gastric surgical procedures..............................................18
Table 1.12 Dietary interventions in the post-gastric surgery
patient (AND, 2015d) ....................................................20
Table 1.13 Potential micronutrient deficiencies following
gastric surgery (O'Donnell 2008) ...................................20
Table 1.14 Foods to include following gastric surgery
(AND, 2015d) ...............................................................21
Table 1.15 Foods to avoid following gastric surgery
(AND, 2015d) ...............................................................22
Table 1.16 Possible nutrition diagnoses related to
constipation (ADA, 2010) ..............................................24
LIST OF TABLES
Table 1.17 Dietary reference intake adequate intake

recommendations for dietary fiber
(Institute of Medicine 2005) .......................................... 25
Table 1.18 Quick estimation for determining daily fiber from
food records (Marlett and Cheung 1997) ....................... 26
Table 1.19 Tips for increasing dietary fiber intake ........................... 27
Table 1.20 Approaches to determine adequate fluid intake
(AND, 2015f)................................................................ 28
Table 1.21 Simple sugars that can cause gas ..................................... 29
Table 1.22 Foods that may produce gas ........................................... 31
Table 1.23 Dietary recommendations for managing diarrhea
(AND, 2015g) ............................................................... 32
Table 1.24 Diet therapies for diverticulosis and diverticulitis ........... 37
Table 1.25 List of low-fiber foods for use in resolving
diverticulitis (AND, 2015h, AND, 2015h) .................... 38
Table 1.26 Nutrition interventions for IBS ...................................... 40
Table 1.27 Nutrition concerns in the person with IBD
(AND, 2015i) ................................................................ 42
Table 1.28 High-oxalate foods to avoid with IBD
(AND, 2015) ................................................................. 44
Table 1.29 Recommended foods for IBD (AND, 2015i) ................. 45
Table 1.30 Foods to avoid with IBD (AND, 2015i) ........................ 46
Table 2.1
Osteoporosis risk factors (NOF, 2015c),

(AND, 2015) ................................................................. 55
Table 2.2
Conditions that increase osteoporosis risk

(AND 2015) .................................................................. 56
Table 2.3
WHO DEXA T-Score result diagnostic criteria

(WHO, 2004) ............................................................... 57
Table 2.4
Dietary reference intakes: recommended dietary

allowances for calcium (Institute of Medicine 2010) ...... 58
Table 2.5
Dairy foods and calcium content (Nelms 2011),

(U.S. Department of Agriculture, Agricultural
Research Service 2012) .................................................. 59
Table 2.6
Nondairy foods and calcium content (Nelms 2011),

Research Service 2012) .................................................. 60
LIST OF TABLES
xi
Table 2.7
Practical method for estimating individual

daily calcium intake ........................................................61
Table 2.8
Calcium supplements .....................................................62
Table 2.9
Vitamin D content of various foods

Research Service 2012) ...................................................63
Table 2.10 Dietary reference intakes for vitamin D

(Institute of Medicine 2010)...........................................64
Table 2.11 Nutrition interview questions for the individual with
rheumatoid arthritis ........................................................69
Table 2.12 Diet therapy for the individual with rheumatoid
arthritis...........................................................................71
Table 2.13 Nutrition interview considerations for the individual
with gout ........................................................................72
Table 2.14 Foods that are low in purines, moderately high in
purines, or very high in purines (AND, 2015c) ...............72
Table 2.15 Nutrition recommendations for acute gout attacks
and between gouty flare-ups (AND 2015a).....................73
Table 2.16 Recommended dietary allowances for iron
(IOM 2001b) .................................................................77
Table 2.17 Factors that limit iron absorption ...................................78
Table 2.18 Approaches to enhancing iron absorption .......................79
Table 2.19 Iron-containing foods (AND 2015d)
Research Service 2012) ...................................................79
Table 3.1
Nutrition supplements recommended for chronic

abusers of alcohol (Markowitz, McRae and Sonne
2000) .............................................................................94
Table 3.2
Five stages of chronic kidney disease (NKF, 2015a) ........99
Table 3.3
Micronutrient regimen for individuals on dialysis

(AND, 2015b)..............................................................101
Table 3.4
High-potassium foods to limit to no more than 1

serving/day (NKF, 2015) ..............................................102
Table 3.5
Low-potassium foods that are appropriate in

moderation for kidney disease (NKF, 2015) .................103
xii
LIST OF TABLES
Table 3.6
How to leach potassium from high-potassium

potatoes, sweet potatoes, carrots, beets, and rutabagas
(NKF, 2015) ............................................................... 104
Table 3.7
How to leach potassium from high-potassium

squash, mushrooms, cauliflower, and frozen greens
(NKF, 2015) ............................................................... 104
Table 3.8
High-phosphorus foods to limit or avoid in CKD

(NKF, 2015) ............................................................... 105
Table 3.9
Lower phosphorus alternatives for high-phosphorus

foods (NKF, 2015) ...................................................... 106
CHAPTER 1
Nutrition and
Gastrointestinal Disorders
Chapter Abstract
A healthy digestive system is imperative for an optimal nutritional status.
Injury or compromise to any segment of the gastrointestinal (GI) tract can
quickly undermine the normal processes of nutrient digestion, transport,
and absorption. As dietetics practitioners are often faced with a wide variety
of GI complaints, the importance of having a thorough understanding of
both the digestive process and the relevant diet therapy for gastrointestinal
disorders cannot be understated. Every year, digestive diseases affects between 60 to 70 million people in the U.S., requiring over 48 million ambulatory visits and 21.7 million hospitalizations. Digestive diseases are
responsible for nearly 250,000 deaths per year and cost $141.8 billion in
indirect and direct medical costs in 2004 (the last year for which cost data
was available) (National Institute of Diabetes and Digestive and Kidney
Diseases 2014).
The term digestive disorders casts a wide net. Because the GI tract
stretches from the mouth to the anus, the probability of something going
awry in this arrangement of anatomy over the course of a lifetime is high.
Underlying disease pathology, medication use, surgical and therapeutic
interventions along with lifestyle choices, and exercise patterns, all impact
gut health. Regardless of the origin or severity of disruption in the GI
tract, dietary alteration is quite commonly a component of digestive disorder management. By understanding the digestive process, where various nutrients are absorbed in the GI tract, and what dietary practices can
be employed to minimize pain and maximize nutritional status, practitioners can help patients use food and nutrition to prevent, manage, and
mitigate a variety of GI disorders. This chapter will introduce the reader
DIET AND DISEASE
to the basics of nutrient digestion, absorption, and transport and then

address a number of disorders of the upper and lower GI tract, for which
evidence suggests that medical nutrition therapy can play a role in preventing, managing or treating them.
Nutrient Digestion, Absorption, and Transport

The process of digesting, absorbing, and transporting nutrients calls on a
great deal of the human anatomy for proper functioning. There are organs
of the digestive tract through which food physically passes as well as organs
which contribute digestive juices, hormones, and enzymes. The organs
which make up the digestive tract consist of the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus. The sections of the
small intestine are the duodenum, jejunum, and ileum. The large intestine,
also called the colon, houses the ascending, transverse, and descending portions of the colon. The pancreas, liver, and gallbladder produce and store
digestive juices and enzymes, and serve as accessory organs to the GI tract.
Select components of the nervous and circulatory systems also play important roles in the digestive process through the creation and dissemination of neurotransmitters and nutrient delivery systems.
Prior to obtaining and utilizing the beneficial nutrients from the
foods consumed, it must first be broken down, or digested, into its most
simple components. The process of digestion allows for the eventual
release, transport, and absorption of nutrients that are vital to health.
The energy-yielding macronutrients (carbohydrate, proteins, and fats)
utilize the digestive process to break their large molecular forms down
into smaller, more usable components as follows:
Carbohydrate digestion involves the breakdown of complex

polysaccharides to form smaller monosaccharides: glucose,
fructose, and galactose.
Protein digestion requires enzymes to break the large
polypeptide proteins down into dipeptides, tripeptides, and
individual amino acids.
Fats are digested down to free fatty acids, monoglycerides,
glycerol, phospholipids, and cholesterol.
NUTRITION AND GASTROINTESTINAL DISORDERS
From a chemical standpoint, digestive juices, or enzymes, are secreted

from the salivary glands, stomach, small intestine, liver (via the gallbladder),
and pancreas. From a physical standpoint, peristalsis and segmentation mediate digestive travel. Peristalsis involves the successive waves of involuntary
muscular contraction in the esophagus, stomach, and small intestine that
move food through the gut. Segmentation is the periodic squeezing or partitioning of the intestine by its circular muscles that mixes and then slowly
pushes the GI contents along.
Muscular sphincters play an important role in regulating the direction
of the flow of chyme in the process of mechanical digestion. Chyme refers
to the bolus of acidic fluid that passes from the stomach to the small intestine and contains gastric juices and partially digested food. The three primary sphincters that are involved in regulating digestive travel and which
prevent backflow of GI tract contents include the following:
Lower esophageal sphincter: located between the bottom of

the esophagus and the top of the stomach; prevents acidic
contents of stomach from splashing back up into esophagus
Pyloric sphincter: located at the bottom of the stomach,
between the stomach and the entrance to the small intestine;
controls the rate of release into small intestine
Ileocecal sphincter: located at the end of the small intestine
and the entrance to the large intestine; prevents contents of
large intestine from re-entering the small intestine
Digestion begins in the mouth, where salivary amylase secreted from

the salivary glands begins to act on the starch content of carbohydratecontaining foods. The chewing and swallowing mechanisms propel the
bolus of food into the esophagus. Food arriving from the esophagus
transits through the lower esophageal sphincter into the stomach where
it mixes with stomach acid and enzymes that promote protein and lipid
digestion. A small amount of lipid digestion take place in the stomach
with the aid of lipolytic enzymes. Here, some proteins are also partially
digested with proteolytic enzymatic assistance and are broken down into
large peptides. The stomach is responsible for the production of gastric
secretions including hydrochloric acid, gastric lipase, mucus, the GI
hormone gastrin, and intrinsic factor (a glycoprotein that promotes absorption of vitamin B12 in the ileum).
DIET AND DISEASE
After its journey through the stomach, the resultant chyme then
transits to the small intestine. The majority of digestion and absorption
of nutrients occurs within the first 100 cm of the small intestine (Mahan
and Escott-Stump 2008). With the exception of fiber and some carbohydrate, digestion and absorption of nutrients is generally completed by
the time food remnants exit the small intestine. The large intestine is the
site of reabsorption of water, electrolytes, and some vitamins. It is here
in the large intestine where food residue remaining after digestion becomes the semisolid waste product called feces or stool. Fecal matter is
stored in the rectum until muscular contractions move the material into
the anal canal in preparation for excretion via the anus.
Nutrient Absorption
No nutrient absorption occurs in the mouth or esophagus. There is a
small amount of absorption that takes place in the stomach, primarily of
alcohol and some medications. The small intestine is where most nutrient
absorption takes place, and the anatomy of the small intestine is uniquely
constructed to maximize nutrient digestion and absorption. The mucosa
of the small intestine is arranged in a pattern of numerous folds that contain fingerlike projections called villi. The villi are constantly moving,
trapping food, and absorbing nutrients. Enterocytes refer to the absorptive
cells that form the outer layer of the villus. Each fingerlike villus projection contains many additional, smaller hairlike projections called microvilli
that also facilitate absorption. The numerous structures of the small intestine increases its capacity for absorption by up to 600 times compared to
that of a simple tube (Wardlaw and Smith 2011).
The process of absorbing nutrients through the wall of the small intestine is dependent on a number of factors such as the type and amount of
nutrient present. Nutrient absorption can occur by simple diffusion, facilitated diffusion, active transport, osmosis, or endocytosis. In simple
diffusion, the nutrient moves down the concentration gradient from the
area of higher concentration in the lumen to the area of lower concentration. This process does not require any energy or protein carriers and is
the process used to absorb many of the water-soluble vitamins, fats, and
some minerals. Facilitated diffusion requires the assistance of a carrier
protein; absorption of the simple sugar fructose is enabled by facilitated

diffusion. Active transport requires a transport protein and energy to
move nutrients against the concentration gradient; glucose and amino
acid absorption rely on active transport. Osmosis refers to the free movement of water across the cell membrane of the enterocytes. Endocytosis is
not a common way in which nutrients are introduced into the enterocytes, but occasionally, as in the case of an infants intestinal tract that can
absorb entire proteins from human milk, part of the cells membrane will
surround and swallow a large protein to aid its absorption.
The small intestine is divided into three sections: the duodenum, the
jejunum, and the ileum. The duodenum is approximately 0.5 meters
long, the jejunum is 2 to 3 meters, and the ileum is 3 to 4 meters. Most
nutrient digestion and absorption occurs in the duodenum and jejunum.
Digestive contents move through the small intestine at a rate of 1 cm per
minute, taking anywhere from three to eight hours to travel the length of
the digestive tract (Mahan and Escott-Stump 2008). Understanding
where nutrients are absorbed along the GI tract can help predict potential nutrient deficiencies when injury or disease afflicts a particular area of
the digestive tract. Table 1.1 outlines the location of specific nutrient
absorption throughout the GI tract.
Table 1.1 Primary sites of nutrient absorption
Organ
Primary nutrients absorbed
Stomach
Water
Alcohol
Minerals: copper, iodide, fluoride, molybdenum
Small intestine
Duodenum Minerals: calcium, phosphorus, magnesium, iron, copper
Vitamins: thiamin, riboflavin, niacin, biotin, folate, vitamins A, D, E, K
Jejunum
Minerals: calcium, phosphorus, magnesium, iron, zinc, chromium,

manganese, molybdenum
Vitamins: thiamin, riboflavin, niacin, pantothenate, biotin, folate, vitamin
B6, vitamin C, vitamins A, D, E, K
Organ
DIET AND DISEASE
Primary nutrients absorbed

Lipids
Carbohydrates: monosaccharides
Proteins: amino acids and small peptides
Ileum
Minerals: Magnesium
Vitamins: vitamin C, B12, D, K, folate
Bile salts and acids
Large intestine
Minerals: sodium, chloride, potassium
Vitamins: vitamin K, biotin
Short chain fatty acids
Water
Nutrient Transport
When nutrients enter the bloodstream or the lymphatic system, they are
transported with the assistance of the circulatory system Blood is carried
to the digestive system via the arteries, which branch into capillaries to
reach every cell in the body. Blood exiting the digestive system travels
via the veins, with the hepatic portal vein directing blood to and from
the liver. The liver is the bodys major metabolic organ, and it plays a
vital role in digestion as it receives and packages absorbed nutrients and
filters out harmful agents.
Lipid absorption proves difficult in the watery environment of the GI
tract, since fats must utilize protein carriers to facilitate their absorption
and transport. The cluster of fat and protein required to transport fats is
called a chylomicron, which is a type of lipoprotein. Chylomicrons move
throughout the body, with surrounding cells picking off their lipid
contents. The shrinking chylomicron eventually travels to the liver,
where different lipoproteins are produced. As a result of this lipid
transport and absorption process, many diseases of the small intestine can
interrupt normal fat digestion and absorption.
The liver produces lipoproteins of varying densities. Very low-density

lipoproteins (VLDLs) are made up primarily of triglycerides, and they
transport lipids to various tissues in the body. Low-density lipoproteins
(LDLs) are derived from VLDLs and are composed primarily of cholesterol. They carry cholesterol and triglycerides from the liver to the cells.
High circulating levels of LDL are thought to elevate risk of cardiovascular
disease. High-density lipoproteins (HDLs) are composed primarily of
protein. They are synthesized in the liver and they take cholesterol from
the cells to the liver in preparation for metabolism and excretion. High
circulating levels of HDL are cardioprotective. Table 1.2 summarizes lipoprotein construction, roles, and health implications, and Chapter 1 of
Diet and Disease I contains more information on lipoproteins and their
role in heart health.
Table 1.2 Lipoproteins, their content, roles in the body and health
implications
Lipoprotein
VLDL:
Very Low-Density
Lipoprotein
...is made
up of
Mostly
triglycerides
LDL:
Low-Density
Lipoproteins
Mostly
cholesterol
HDL:
High-Density
Lipoproteins
Mostly
protein
Health
implications
...and does:
Takes triglycerides
(TG) from liver to
body tissues
Made by liver
Carries cholesterol
and TG from liver to

body cells
What is left after cells

remove TG from
VLDLs
Carries cholesterol
back to the liver from
the bodys cells
Large, light, and

lipid-filled
LDL linked to
heart disease risk
LDL = Bad (Lesshealthy) cholesterol
Small, dense, and
protein-packed
HDL thought to
be cardioprotective
HDL = Good
(Healthy)
cholesterol
DIET AND DISEASE
Medical Nutrition Therapy for Disorders

of the Upper GI Tract
Dry Mouth
Dry mouth, also called xerostomia is a common salivary gland disorder.
An individual with healthy salivary glands will produce between one and
two liters of saliva per day. Saliva is almost entirely made up of water
(99.5 percent), electrolytes, and protein. Saliva is secreted from the salivary glands and it contains amylase, an enzyme that initiates starch
breakdown in the mouth. It is also responsible for the lubrication and
moistening of food in preparation for digestion. Saliva is vital for dental
hygiene because it neutralizes acid, protects teeth from dental caries,
washes food away from the oral cavity, and facilitates the bacteriolytic
protein lysozyme that further protects dentition from bacteria.
Xerostomia is a common side effect of a number of conditions, including Parkinsons disease, HIV/AIDS, Sjgrens syndrome, poorly controlled
diabetes, and other autoimmune illnesses (Atkinson and Wu 1994).
Advancing age, radiation therapy and chemotherapy, nerve damage to the
head or neck, and many medications can result in dry mouth. Prolonged
xerostomia can interfere with speech, swallowing and taste. It promotes
plaque formation, results in halitosis, contributes to depression, and negatively affects food intake and nutritional status. Patients often decrease the
variety of foods they eat due to the discomfort associated with dry mouth
(Eisbruch 2007).
When xerostomia as a side effect can be predicted, focusing on prevention should be the key, being mindful that nutrition, lifestyle, and
pharmacologic treatment may also be indicated. Prevention (including
products and practices to avoid) and treatment recommendations are
outlined in Table 1.3.
Table 1.3 Xerostomia treatment techniques and products to avoid
(AND, 2015)
Nutrition &
lifestyle
Artificial saliva
Gum chewing
Oral care
practices
Pharmacologic
Amifostine
Inorganic
Mouth rinse: to
1 teaspoon
Products to
avoid
Sucrosecontaining &
Nutrition &
lifestyle
Sugarless candy
Increased fluid
intake/frequent
sips of water
Sucking on ice
cubes
Consumption of
foods with high
fluid content
Use of
humidifier
during sleep
Oral care
practices
Pharmacologic
thiophosphate,
broad-spectrum
cytoprotectant
Artificial saliva;
available as sprays,
lozenges, gels, and
swabs
baking soda + 8
ounces water
every 2 hours
while awake
Biotene products
by Laclede, Inc.;
include
toothpaste,
mouth rinse,
chewing gum
Chapstick and
moisturizing gels
to lips
Pilocarpine
Products to
avoid
carbohydrates
that stick to
teeth & lead to
dental caries
Citrus & spicy
foods
Dry and hard,
non-moist
foods
Caffeine; limit
coffee & tea
Tobacco
Alcohol
Alcohol-based
mouth washes
Dysphagia
Proper swallowing is a complex action that requires the adequate functioning of a number of pieces of anatomy. The term dysphagia refers to
difficulty with swallowing or improper swallowing. Dysphagia is not a
specific diagnosis or disease, but rather, the disruption of swallowing
that may be an indicator or symptom of any one of a number of disorders. Oropharyngeal dysphagia refers to the inability to transfer food
from the mouth and pharynx to the esophagus. This is usually caused by
a neuromuscular disorder that disrupts the swallowing reflex or renders
the muscles involved in swallowing unable to move. Signs of oropharyngeal dysphagia include presence of a gurgling noise following swallow, a
hoarse or wet voice or a resultant speech disorder. This is the type of
dysphagia that is commonly seen in the elderly following a stroke.
Esophageal dysphagia refers to interference with the actual passage of
food or beverage down the esophagus and into the stomach. This may
occur as a result of an obstruction in the esophagus or a motility disorder. People with esophageal dysphagia often complain of food getting
stuck in the esophagus following swallow. The obstruction may be the
result of a stricture, tumor or compression of the esophagus due to impairments in surrounding anatomy.
10
DIET AND DISEASE
Table 1.4 Nutritional consequences of untreated dysphagia

(AND, 2015a)
Negative nutritional impacts of untreated dysphagia
Malnutrition
Aspiration pneumonia
Dehydration
Unintended weight loss
Depression
Mortality
Pneumonia
Decreased rehabilitation potential
Decreased quality of life
Increased length of hospital stay
Increased costs
Dysphagia can negatively impact nutritional status if it affects dietary intake. Complications of dysphagia include choking and aspiration.
Reduced ability to swallow food safely can result in a variety of nutritional deficiencies. Potential nutritional impacts of untreated dysphagia
are outlined in Table 1.4.
Nutritional Management of Dysphagia

Determination of safe swallow prognosis in patients with dysphagia involves a team-based clinical approach, with the speech language
pathologist ultimately determining the appropriate level of modified diet
texture and liquid consistency. The nutritional management of dysphagia generally involves manipulation or modification of foods and beverages to make them easier to swallow. The National Dysphagia Diet
(NDD) was developed in 2002 and sought to standardize the nutrition
care of dysphagia patients. NDD proposes four levels of semisolid and
solid foods, and outlines inclusion and exclusion food items for each
level. Table 1.5 provides the specifics of the NDD.
11
Table 1.5 The National Dysphagia Diet food considerations

(McCallum 2003), (McCullough, Pelletier and Steele 2003)
The national dysphagia diet
The National Dysphagia Diet (NDD) is a standardized set of terminology for a progressive
diet used nationally in the treatment of dysphagia. The NDD outlines requirements for
both food consistency and liquid viscosity.
Dysphagia pureed (NDD 1)
Smooth, pureed, homogenous, cohesive foods of pudding-like consistency

Mashed potatoes should be served with gravy, butter, margarine or sour cream
Pre-gelled slurried breads are allowed
Avoid gelatin, fruited yogurt, unblenderized cottage cheese, peanut butter, lumpy food
including hot cereal and soup
Avoid scrambled, fried or hard-boiled eggs; souffls are allowed
Dysphagia mechanically altered (NDD 2)
Moist, soft-textured foods that easily form a bolus

Moist, tender ground or finely diced meats
Soft, tender-cooked vegetables and soft ripe or canned fruit
Slightly moistened dry cereal with little texture
Meats should not exceed in. cube, moisten with gravy or sauce
Allows canned fruit (except stringy pineapple), cooked fruit or fresh banana
Allows scrambled, poached, or soft cooked eggs
Cooked vegetables should be less than in. and fork mashable
No bread, dry cake, rice, cheese cubes, corn, or peas
Avoids skins, dry fruit, coconut, and seeds
Note: Mechanical soft diet includes same foods as above, but allows bread, cakes and
rice
Dysphagia advanced (NDD 3)
Food is nearly regular texture with the exception of very hard, sticky, or crunchy foods
Allows breads, rice, moist cakes, shredded lettuce, and tender moist whole meats
Avoids hard fruits and vegetables, corn, skins, nuts, and seeds
Regular
All foods are allowed
Dysphagia affects not only solid food swallowing capabilities but also
the ability to safely swallow liquids of varying consistency. NDD proposes
four frequently used terms to label levels of liquid viscosity. Speech language
pathologists determine the viscosity of fluid that a patient can tolerate separately from solid food recommendations. The classification of liquid types is
12
DIET AND DISEASE
Table 1.6 National Dysphagia Diet liquid consistencies

(AND, 2015a)
NDD liquid
consistency
Inclusions
Thin liquid
Regular liquids, no adjustments

Includes anything liquid at room temperature: frozen yogurt, ice
cream, popsicles
Includes clear juices, milk, water, tea, coffee, soda, broth, plain
gelatin, high-liquid fruits such as watermelon, grapefruit, and
orange sections or any food that will liquefy in the mouth within
a few seconds
Nectar-like
Falls slowly from a spoon and can be sipped through a straw or cup
Includes nectars, vegetable juices, chocolate milk, buttermilk,
thin milkshakes, cream soups, other properly thickened beverages
Honey-like
Drops from a spoon and is too thick to be sipped from a straw

Includes tomato sauce
Spoon-thick
Maintains shape, needs to be taken with a spoon, and too thick

to drink
Includes pudding, custard, hot cereal
based on measurements using a viscometer. As most commercial establishments do not have a viscometer, commercial thickening agents are generally
used to achieve the appropriate level of thickness. The four liquid types in
the NDD are presented in Table 1.6, in order of least restrictive to most
restrictive.
Dehydration risk increases with dysphagia because fluid intake is often limited or suboptimal. While an individuals fluid needs are dictated
by disease state, a general rule of thumb is that 30 mL of fluid per kilogram of body weight will provide normal daily fluid requirements. Fluid
requirements may vary for those with cardiac problems, renal failure,
dehydration, obesity, or in those who require fluid restrictions (AND,
2015a).
Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) occurs when the contents of
the stomach splash back up into the esophagus causing irritation and a
burning sensation. Compromised lower esophageal sphincter (LES)
13
pressure can allow the acidic contents of the stomach to re-enter the
esophagus, causing dysphagia, heartburn, belching, and increased salivation (Nelms 2011). Because the lower esophageal sphincter serves as the
gateway between the lower portion of the esophagus and the upper
compartment of the stomach, any compromise to the sphincter muscle
may result in reflux. GERD is more commonly seen during pregnancy,
in obese individuals, and those with hiatal hernia (a condition wherein
the top part of the stomach protrudes above the diaphragm).
The presence of gastric acid in the esophagus can impair the esophageal lining, resulting in inflammation called reflux esophagitis. Prolonged
inflammation can cause esophageal ulcers, which in turn may bleed and
cause pain. When ulcerated tissue eventually heals, it can cause scarring
which will narrow the inner lumen of the esophagus and further restrict
access. Aspiration is a risk and lung disease may occur if food is aspirated
into the lungs. Chronic exposure to acid in the esophagus can lead to
Barretts esophagus, a condition characterized by esophageal cells that are
damaged by exposure to stomach acid becoming replaced by cells similar
to those in the stomach or small intestine and that are occasionally cancerous. Other consequences of GERD include damage to tissue in the
mouth, erosion of tooth enamel, sore throat, cough, and laryngitis (Falk
and Katzka 2012).
Nutritional Management of GERD

In addition to the use of medications to manage GERD, nutrition therapy
may also be employed to help lessen symptoms and prevent flare-ups. The
nutritional management of GERD includes avoidance of foods and agents
that reduce lower esophageal sphincter pressure, restriction of foods that
increase gastric acidity and improvement of clearance of contents from the
esophagus. Specific recommendations for intervention goals and diet therapy for patients with GERD can be found in Tables 1.7 and 1.8.
14
DIET AND DISEASE
Table 1.7 Nutrition interventions and goals in patients with GERD

(AND, 2015b)
Nutrition intervention goals for patients with GERD
Improve competence of lower esophageal sphincter
Decrease gastric acidity
Improve clearance of esophageal contents
Initiate weight loss if indicated
Identify potential drug-nutrient interactions
Prevent obstruction if esophageal stricture present
Improve overall nutrition intake
Table 1.8 Diet therapy for patients with GERD (AND, 2015b),
(Hasler 2015)
Diet therapy for GERD
Restrict foods that increase gastric acidity, including black pepper, red pepper, coffee
(includes decaffeinated), and alcohol.
Eliminate foods and agents that reduce lower esophageal sphincter pressure, including
chocolate, mint, high-fat foods, and tobacco.
Lose weight if indicated.
Stop smoking.
Refrain from lying down after eating; remain upright.
Restrict eating within three hours of bedtime.
Avoid tight-fitting clothing.
Elevate head of bed while sleeping.
Substitute large, high-fat meals with smaller, more frequent lower-fat meals.
Hiatal Hernia
As mentioned previously, a hiatal hernia occurs when the top portion of
the stomach and the lower esophageal sphincter protrude through the
esophageal hiatus into the thoracic cavity. The presence of a hiatal hernia
facilitates easy reflux of acid into the esophagus. Hiatal hernia symptoms
are similar to those of GERD, and the primary dietary interventions for
GERD also apply (see Tables 1.7 and 1.8). Because hiatal hernias and
15
associated GERD are more prevalent in the obese, weight loss efforts
should be undertaken if indicated (Barak et al., 2002). Those with hiatal
hernias should be advised to avoid high-fat meals and to avoid laying
down less than three hours after eating.
Peptic Ulcer Disease

Peptic ulcer disease (PUD) is characterized by ulceration in the gastric
and duodenal mucosa. In the United States, more than 15.5 million
people have the condition and nearly 3,000 will die each year from PUD
(National Institute of Diabetes and Digestive and Kidney Diseases
2014). Ulcers are five times more likely to occur in the duodenum than
in the stomach. Understanding the etiology of and approach to treating
PUD has changed dramatically since Helicobacter pylori infection was
identified as a primary factor in its development (Chey and Wong 2007).
It is now believed that 70 percent of gastric ulcers and 92 percent of duodenal ulcers are caused by H. pylori (Makola, Peura and Crowe 2007).
The use of nonsteroidal, anti-inflammatory drugs (NSAIDs), aspirin, and
corticosteroids may also contribute to the development of PUD.
Medication and Nutritional Management of Peptic Ulcer Disease

Medication use remains the preferred treatment modality for PUD;
however, diet and lifestyle choices can alleviate PUD-associated pain.
The medication treatment regimen for H. pylori infection usually involves three or four drugs. Acid suppression is achieved with a proton
pump inhibitor (PPI) alongside antibiotic therapy and use of a bismuthcontaining agent, such as Pepto-Bismol (Schafer 2012). In addition to
medication, diet and lifestyle choices can ameliorate PUD-associated
pain. The approach to non-medication-related management of PUD
focuses on three strategies: (1) avoiding and/or treating factors that impair mucosal integrity, (2) avoiding behaviors that reduce blood flow to
the gastric and duodenal mucosa, and (3) avoiding factors and foods
that stimulate excessive gastric secretions. Table 1.9 outlines the specifics
of these three approaches.
16
DIET AND DISEASE
Table 1.9 Factors that exacerbate peptic ulcer disease (AND, 2015c)
Factors that may affect mucosal integrity
Helicobacter pylori infection

Aspirin
Nonsteroidal, anti-inflammatory drugs (NSAIDs)
Alcohol
Steroids
Factors that decrease blood supply to gastric or duodenal mucosa
Smoking
Stress
Injury (e.g., Curlings ulcer in a burn injury)
Factors that increase acid secretion
Foods including pepper, alcohol and caffeine from colas,
coffee, decaffeinated coffee, tea, and chocolate
Rapid gastric emptying
Stress
Other conditions (e.g., Zollinger-Ellison syndrome)
Peptic ulcer-associated pain can impede nutritional intake and reduce appetite, resulting in unintended weight loss and potential nutrient
deficiencies. Iron deficiency can occur as a result of blood loss. Longterm use of medications that suppress acid secretion can lead to suboptimal absorption of calcium, iron, and vitamin B12 (Yang et al., 2006),
(O'Connell et al., 2005).
Abdominal discomfort with PUD generally occurs when the stomach
is empty. Common complaints include feelings of an upset stomach and
dull or burning pain either between meals or during the night. In the case
of duodenal ulcers, food is likely to help relieve the pain. Antacid use can
alleviate pain with both gastric and duodenal ulcers. Patients should be
encouraged to identify and avoid foods that are not well tolerated or that
easily irritate the gastric mucosa. In addition to individualized food recommendations, all people with PUD should be advised to avoid foods
that may increase gastric acid secretion or that are known to harm the
gastric mucosa, including pepper, alcohol, and caffeine from colas, coffee,
decaffeinated coffee, tea, and chocolate.
17
Table 1.10 Foods not recommended for people with peptic ulcer
disease (AND, 2015c)
Food groups
Foods not recommended
Milk & Milk Products
Whole milk
Cream
Dairy products from whole milk or cream
Chocolate milk
Meat & Other Protein Foods High-fat meats

Meats not tolerated on an individual basis
Beverages
Cola
Coffee (including decaffeinated)
Green or black tea (including decaffeinated)
All caffeinated beverages
Alcohol
Fat & Oils
Butter
Lard
Stick margarine
Hydrogenated oils
Fried foods
Spices
Pepper
Encouraging small, frequent meals, avoiding fried foods, and smoking cessation are advisable for PUD. Many individuals find that avoiding food for at least two hours before bedtime also helps minimize
PUD-associated discomfort. Previous diet therapy was based on the notion that milk and milk products could coat the stomach and protect
against gastric secretions, a therapy formerly called the sippy diet. It is
now known that milk, with its protein content, actually increases gastric
secretions. Generally, with active PUD, reduced-fat (2%) milk, whole
milk, cream, chocolate milk, and high-fat yogurt are discouraged
(Nelms 2011), (AND, 2015c). If tolerated, some patients may wish to
include nonfat (skim) milk, low-fat (1%) milk, buttermilk, or low-fat
and nonfat yogurt. Table 1.10 outlines foods that are to be avoided or
minimized in individual with PUD.
18
DIET AND DISEASE
Gastric Surgery
An individual may require gastric surgery for one of a number of reasons: malignancy, PUD, or surgical weight loss. Regardless of the diagnosis or condition necessitating gastric surgery, understanding how such
Table 1.11 Gastric surgical procedures
Gastric surgery
procedure
Anatomical effects
Vagotomy
Eliminates innervations from the vagus nerve to parietal cells

Results in decreased acid production
Results in decreased response to gastrin
Pyloroplasty
Innervations to parietal cells are severed

Eliminates part of the vagus nerve that controls gastric emptying
Pyloric sphincter is enlarged
Billroth I
Partial gastrectomy or pyloroplasty performed with reconstruction

with anastamosis of proximal end of the duodenum to distal end of
the stomach
Bilroth II
Partial gastrectomy with anastamosis of the proximal end of the

jejunum to the distal end of the stomach
Roux-en-Y
Partial gastrectomy with creation of a small pouch and anastomosis

of jejunum to the upper part of the stomach
surgeries impact nutrient digestion and absorption can help predict where
particular nutrient deficiencies or deficits may arise. Patients undergoing
gastric surgery are at increased nutritional risk from potentially poor oral
intake, maldigestion, and malabsorption of nutrients. Table 1.11 provides
a brief overview of the various surgical procedures.
Normal digestive processes are disrupted with any gastric surgery,
either by reducing the capacity of the stomach or altering the transit
time for contents in the gut. Altering the normal digestive process in the
stomach leads to resultant reduction in the production of intrinsic
factor. Intrinsic factor is produced by the parietal cells of the stomach
and is required for optimal vitamin B12 absorption. Gastric surgery
often results in suboptimal vitamin B12 status due to reduced intrinsic
factor. Hydrochloric acid (HCl) production is also affected by gastric
surgery, resulting in further disruption of the normal digestive process.
19
Furthermore, bone health suffers as calcium absorption is compromised,

resulting in an increased need for calcium and vitamin D supplementation in the post-surgical state.
Dumping Syndrome
Dumping syndrome is a cluster or symptoms resulting from the rapid
emptying of an osmotic load from the stomach into the small intestine;
it is a common side effect of gastric surgery. Dumping syndrome can be
initiated by alterations in the rate of gastric emptying, innervation to the
stomach, and fluctuating stimulation of GI hormones. If normal gastric
emptying rates cannot be achieved, a higher osmotic load dumps into
the small intestine too quickly, which results in much more volume than
can be comfortably accommodated.
Dumping results in abdominal cramping and pain, diarrhea, dizziness,
weakness, and tachycardia. These symptoms are present in early dumping
syndrome, occurring within the first 10 to 20 minutes following a meal.
Undigested food then moves to the large intestine, where colonic fermentation produces gas, abdominal pain, cramping, and diarrhea. Late dumping
syndrome takes place between one and three hours following food intake,
particularly after the consumption of simple carbohydrates. The rapid rate
of absorption in the small intestine stimulates insulin release. Insulin, in the
presence of hypermotility and decreased transit time, finds no remaining
substrate on which to act, causing subsequent hypoglycemia. The symptoms of hypoglycemia, and ultimately, late dumping syndrome, include
confusion, weakness, shakiness, and sweating (AND, 2015d).
Dumping syndrome can be managed by dietary modification. Eating small and frequent meals, avoiding simple carbohydrates (including
clear liquids with simple sugars), drinking fluids separate from solid
foods, and incorporating supplemental pectin or guar gum to promote
increased viscosity of food can all help minimize symptoms. The presence of sugars and sugar alcohols in the GI tract may exacerbate associated GI symptoms. As such, patients are generally advised to avoid sucrose, fructose, and sugar alcohols such as sorbitol, mannitol, and xylitol
(ingredients often found in sugar-free and diet foods, candies, chewing
20
DIET AND DISEASE
gum, and drinks). Contrary to other GI-related nutrition therapies,

those with dumping syndrome may benefit from laying down following
meals. Table 1.12 highlights recommended dietary interventions for the
post-gastric surgery patient intended to maximize nutrient status and
avoid dumping syndrome. Table 1.13 outlines the micronutrients of
concern in the post-gastric surgery patient, while Table 1.14 contains
foods to include following gastric surgery and Table 1.15 provides information about foods to avoid following gastric surgery.
Table 1.12 Dietary interventions in the post-gastric surgery patient
(AND, 2015d)
Dietary interventions in the post-gastric surgery patient
Avoid simple sugars (sucrose, fructose), sugar alcohols (sorbitol, mannitol, xylitol), and
clear liquids (except broth) at the first feedings.
First meal post-surgery should contain protein, fat, and complex carbohydrate, and be
limited to only one to two food items at a time.
Include non-lactose containing sources of calcium as patients may experience lactose
intolerance from foods.
Slowly progress to five to six small meals per day.
Drink liquids thirty minutes to one hour after eating solid food.
Lay down after eating.
Utilize functional fibers to delay gastric emptying and to mitigate diarrhea.
Liquid multivitamin and mineral supplements should be used to meet minimum nutrient
needs.
Begin vitamin B12 injections .
Table 1.13 Potential micronutrient deficiencies following gastric

surgery (O'Donnell 2008)
Potential micronutrient deficiencies
following gastric surgery
Iron
Copper
Folate
Thiamin
Calcium
Vitamin A
Vitamin B12
Vitamin D
21
Table 1.14 Foods to include following gastric surgery (AND, 2015d)

Foods to include after gastric surgery
Milk and dairy foods
Recommended foods: buttermilk, evaporated and skim, 1% milk, soy milk without added
sugar, yogurt without added sugar, powdered milk, cheese, low-fat, low-sugar ice cream
Select lactose-free foods following surgery.
Choose yogurts that contain live, active cultures (but without added sugars).
Drink milk and other liquids between meals, rather than with food.
Wait 3060 minutes after eating solid foods to try beverages.
Meat and protein foods
Recommended foods: tender, well-cooked meats, poultry, fish, eggs, smooth nut butters or
soy foods made without added fats
Include a protein food at every meal and snack.
Grains
Recommended foods: white breads, bagels, rolls, crackers and cold or hot cereals made
from refined wheat or white flour
Look for grains that have less than two grams of fiber per serving.
Choose cereals with no added sugar.
Vegetables
Recommended foods: most well-cooked vegetables without seeds or skins, potatoes without
skin, lettuce, or strained vegetable juice
Fruits
Recommended foods: canned, soft fruits without added sugar, bananas, melons
Fats
Recommended foods: small amounts of oils, butter, margarine, cream, cream cheese, and
mayonnaise
Beverages
Recommended foods: decaffeinated coffee, caffeine-free tea, and caffeine-free sugar-free
sodas
Do not drink beverages with meals.
Sweeten beverages only with artificial sweeteners, not sugar-containing sweeteners.
Sweeteners
Recommended foods: artificial sweeteners, and foods or beverages that contain them
Instead of sugar, choose artificial sweeteners such as Sweet'N Low, Equal, NutraSweet,
Splenda, Stevia, Sunnette, or Sweet One
22
DIET AND DISEASE
Table 1.15 Foods to avoid following gastric surgery (AND, 2015d)

Foods to avoid after gastric surgery
Milk and dairy foods
Chocolate milk
Any milk with added sugar
Avoid regular milk if you have lactose intolerance
Meat and protein foods
Fried meat, poultry or fish
Lunch meats like bologna or salami
Sausage, hot dogs, bacon
Tough or chewy meats
Dried peas and beans like pinto or kidney beans
Chunky nut butters or nuts
Vegetables
Any raw vegetables except for lettuce
Any cooked vegetables served with skins or seeds
Beets
Broccoli, Brussels sprouts, cabbage
Cauliflower
Collards, mustard, turnip greens
Corn
Potato skins
Fruits
All raw fruits except for bananas and melons
All dried fruits including prunes and raisins
Fruit juice
Canned fruit packed in sugar or syrup
Beverages
Caffeinated coffee or tea
Alcoholic beverages
23
Foods to avoid after gastric surgery

Beverages made with sugar, corn syrup, or honey
Fruit juices and fruit drinks
Do not drink beverages with meals and snacks; rather, wait 3060 minutes after food to
drink
Sweeteners
Sugar
Honey, syrup
Sugar alcohols such as sorbitol or xylitol
Foods that list sugar, honey, syrup, xylitol or sorbitol as one of the first three ingredients
Medical Nutrition Therapy for Disorders

of the Lower GI Tract
The lower section of the gastrointestinal tract is of incredible importance
when it comes to the optimal digestion, absorption, and transport of nutrients. It is here in the lower half of the GI tract, the small intestine, large intestine, colon, and anus that 98 percent of all digestion and absorption takes
place (Nelms, Diseases of the Lower Intestinal Tract 2011). In essence, the
lower GI tract finishes what the upper GI tract started: movement of GI
contents, secretion of digestive enzymes and juices, and nutrient digestion,
absorption, and transport.
The small intestine consists of three segments: the duodenum, jejunum, and ileum. Most digestion occurs in the duodenum and the upper
section of the jejunum. The arrangement of intestinal tissue folds within
the small intestine is uniquely suited to maximizing nutrient absorption.
The folds are covered in small, fingerlike projections called villi. Each
villus is covered in another tiny layer of absorptive cells called enterocytes. A part of the enterocyte is exposed to chyme, or the by-products
of digestion. This end, often referred to as the brush border is in turn
covered in many hairlike projections called microvilli. The microvilli
house brush border enzymes that facilitate the digestion of protein and
carbohydrate.
24
DIET AND DISEASE
Table 1.16 Possible nutrition diagnoses related to constipation

(ADA, 2010)
Possible nutrient diagnosis related to constipation
Inadequate fluid intake
Inappropriate intake of carbohydrates
Inadequate dietary fiber intake
Undesirable food choices
Food and nutrition related knowledge deficit
Constipation
The American Gastroenterological Association maintains that it is not
necessary to have at least one bowel movement per day. They define regular motility as having from three bowel movements per day to three per
week (AGA, 2013). Constipation can arise from a lack of dietary fiber or
as a secondary occurrence related to another condition or disease. Common causes of constipation include obesity, pregnancy, inactivity, and
irritable bowel syndrome. Less common causes may include laxative
abuse, hormonal disturbances, loss of body salts, mechanical compression,
nerve damage, or other diseases such as diabetes, Parkinsons disease, multiple sclerosis, stroke, spinal cord injuries, disorders of the thyroid gland,
lupus, and scleroderma. Medication may induce constipation, with diuretics, calcium or aluminum antacids, pain medications containing codeine, antidepressants, antihistamines, and iron and calcium supplements
being particularly constipating (AND, 2015e). The use of fiber supplements without adequate fluid intake may also contribute to constipation.
Table 1.16 contains potential nutrition diagnoses for constipation.
Dietary Fiber and Constipation

The most well-known association between constipation and diet pertains
to the inadequate intake of dietary fiber. Different guidelines and professional bodies tout different fiber recommendationsand although the
recommended amount of fiber may differ, they are all higher than the
average U.S. daily fiber intake, which currently stands at 13 to 15 grams
25
per day (King, Mainouse and Lambourne 2012), (Alaimo et al., 1998).
The Institute of Medicines Dietary Reference Intake (DRI) for fiber is
based on 14 grams per 1,000 calories consumed (Institute of Medicine
2005). Based on the DRI recommended calorie intake levels, this level is
25 grams per day for adult women and 38 grams for men. Table 1.17
contains the DRI for fiber for different age and gender groups (Institute
of Medicine 2005).
Gathering accurate data about average fiber intake may be challenging in the clinical environment; however, taking a quick survey of a persons previous 24-hour intake can yield substantial information about
the nature (or absence) of dietary fiber in the diet. Diets that are low in
fiber also tend to be low in fruits, vegetables, whole grains, and legumes.
These same diets tend to be high in dairy, meat, refined carbohydrate
foods, and fats. While it is the insoluble fibers that appear to have the
greatest effect on constipation, there is no clear evidence with regards to
the best type of fiber to alleviate constipation (Tan and Seow-Choen
2007). Insoluble fibers are found in the skins of fruits and vegetables,
and in whole grains. Table 1.18 offers a quick way to estimate fiber intake from a persons food record.
Table 1.17 Dietary reference intake adequate intake

recommendations for dietary fiber (Institute of Medicine 2005)
Daily fiber intake recommendations for children
Babies 06 months: no fiber recommendations

Babies 712 months: not enough data to set recommended level
Children 13 years: 19 g of fiber per day
Children 48 years: 25 g of fiber per day
Children 913 years: girls need 26 g and boys need 31 g per day
Adolescents 1418 years: girls need 26 g and boys need 38 g per day
Daily fiber intake recommendations for adults
Female adults age 50 and younger: 25 g of fiber per day

Female adults age 51 and older: 21 g of fiber per day
Male adults age 50 and younger: 38 g of fiber per day
Male adults age 51 and older: 30 g of fiber per day
26
DIET AND DISEASE
Table 1.18 Quick estimation for determining daily fiber from food
records (Marlett and Cheung 1997)
To quickly estimate fiber intake from a food record:
1. Multiply number of fruit and vegetable servings by 1.5 g.
2. Multiply number of servings of whole grains by 2.5 g.
3. Multiply number of servings of refined grains by 1.0 g.
4. Add specific fiber amounts for nuts, legumes, seeds, and high-fiber cereals.
5. Total to estimate fiber intake per day.
Rather than expend unnecessary energy making specific soluble versus

insoluble recommendations, the nutrition practitioner is instead advised
to encourage an overall, gradual intake of any and all dietary fiber from
food sources. A well-balanced diet with fiber-containing foods will naturally have both soluble and insoluble fiber content. Individuals should be
cautioned that a sudden and intentional increase in dietary fiber intake
may result in undesirable GI side effects. People with constipation should
be advised to gradually increase their fiber intake, increasing intake by no
more than a few grams per day, and to always ensure adequate fluid intake
along with increasing intake of fiber. Increasing fiber intake too quickly or
without adequate fluid intake can cause gas, bloating, cramping, diarrhea,
and general GI discomfort.
Functional Fibers
Encouraging individuals to increase their dietary fiber intake can be a challenging undertaking in todays food environment. As consumers interest in
fiber grows, so do food manufacturers offerings of fiber-containing packaged and processed foods. Isolated are being increasingly added to many
packaged and processed foods that are normally low in fiber. They contain
ingredients such as maltodextrin, oat fiber, resistant starch, pectin, gum,
polydextrose, and inulin (from chicory root), among others. In high concentrations, these additives may cause gastrointestinal distress in some individuals (Bonnema et al., 2010), (Storey et al., 2007) although they may be
tolerated at lesser levels by others (Stewart et al., 2010).
27
Table 1.19 Tips for increasing dietary fiber intake

Tips for increasing dietary fiber intake
Leave skins and peels on fruits and vegetables.
Use 100% whole wheat bread instead of wheat or white bread.
Try 100% whole wheat pasta or brown rice.
Replace half of white flour in baking with a whole grain flour.
Look for breads and cereals that have the word whole in their first ingredient.
Steam vegetables quickly to retain color and crunch.
Utilize low-sodium canned beans in casseroles, salads and soups.
Explore whole grains: try barley, quinoa, wheat berries, or whole wheat couscous.
Add cup cut fruit to your cereal, oatmeal, or yogurt.
Use fruit as a between meal snack: aim for three servings of fresh or frozen fruit per day.
On the topic of functional fibers, the Academy of Nutrition and Dietetics maintains in its position paper that, [w]hether isolated, functional
fibers provide protection against cardiovascular disease remains controversial. The paper goes on to say, longer-term studies of fiber intake which
examine the effects of both intrinsic [intact] and functional [isolated]
fibers are required (ADA, 2008).
Nutrition practitioners should work with clients to increase dietary
fiber intake from naturally occurring sources of dietary fiber as opposed
to synthetic fibers added to processed foods. Naturally occurring sources
of fiber include fresh and frozen fruits and vegetables, whole grains,
dried peas and beans, and lentils. When choosing bread products made
with flour, counsel patients and consumers to look for the word whole
in the first ingredient in the ingredient list. Avoid bread products with
enriched wheat flour as the first ingredient, as these are made with
refined, low-fiber wheat flour. Table 1.19 contains additional tips for
increasing dietary fiber from food (and not supplement) sources.
Fluid Intake and Constipation

Alongside inadequate dietary fiber intake, insufficient fluid can exacerbate
underlying constipation. While there are no consensus guidelines for fluid
intake recommendations, some bodies recommend increasing fluid intake
28
DIET AND DISEASE
to at least 64 ounces (eight cups) per day (AND, 2015e). The best indicator of hydration status is urine color: light yellow or clear urine that is not
pungent indicates adequate hydration in most cases. Urine that is dark
yellow or orange and urine that has a pungent odor indicates the presence
of concentrated waste product and insufficient hydration status.
Three other ways of estimating fluid needs are based on calorie intake, body weight, or calorie intake plus nitrogen consumed. Providing
one mL of fluid per calorie consumed per day is estimated to meet hydration needs in otherwise healthy people. Alternatively, providing 35 to
40 mL/kg for people aged 16 to 30, 30 to 35 mL/kg for healthy adults,
30 mL/kg for those 55 to 65 years old, and 25 mL/kg for those over 65
can also meet fluid needs. Lastly, a less commonly used practice bases
fluid recommendations on nitrogen and energy intake by providing
1 mL/kcal + 100 mL/g nitrogen consumed (AND, 2015f). Table 1.20
summarizes a variety of approaches to estimate daily fluid requirements.
Table 1.20 Approaches to determine adequate fluid intake
(AND, 2015f)
Approaches to determine adequate fluid intake
Observe color of urine
Clear or light yellow indicates adequate hydration.

Dark yellow or orange or pungent smelling urine indicates dehydration.
Cups per day
Ideal goal is 64 oz. or eight 8 oz. cups per day.
Based on energy intake
1 mL fluid per kcal ingested
Based on body weight
Age 1630, give 3540 mL/kg/day fluid

Healthy adults, give 3035 mL/kg/day fluid
Adult aged 5565, give 30 mL/kg
Adult >65 years, give 25 mL/kg
Based on nitrogen and energy intake
1 mL/kcal + 100 mL/g nitrogen (g protein divided by 6.25 = nitrogen)
Fluid balance method
Urine output + 500 mL per day
29
Physical Activity and Additional Approaches to Combatting

Constipation
A sedentary lifestyle goes hand in hand with constipation. Inactivity is often
the culprit of such problems in the elderly or those confined to bed. Nutrition prescriptions for constipation should include recommendations to participate in daily physical activity. Traditional nutrition interventions for
constipation involve increasing fiber in the diet, increasing fluid intake
throughout the day, manipulating medication routines if necessary, and
promoting regular physical activity. Including probiotics and prebiotics
daily may prove helpful in some situations, as can the use of bulk-forming
agents such as psyllium, calcium polycarbophil, or methylcellulose. It is
important to note that those who are reliant on laxatives may not respond
to fiber treatment (Schiller 2008).
Intestinal Gas
As is the case with constipation, the presence of gas and flatulence may
be caused by either an underlying condition or as a result of a separate
therapeutic medication or treatment. Foods and agents that cause gas
vary greatly between individuals; and because of the highly individualized nature of such a condition, there is not one given therapy that will
be beneficial for all who experience this uncomfortable GI problem.
Gas can be caused by one of two things: from the swallowing of air or
from the breakdown of certain undigested foods by colonic bacteria. The
best nutrition advice for gas and flatulence is also the simplest: avoid the
offending food or foods. Gas-causing foods include simple sugars, starches,
and fiber (Shepherd et al., 2008). Simple carbohydrates that are known to
be gas inducing, and their sources can be found in Table 1.21.
Most starches give off gas as they are broken down in the large intestine; rice is the only starch known to not cause gas (National Digestive
Diseases Information Clearing House 2013). Dietary fiber, despite its
varied benefits can contribute to gas. Soluble fiber, found in foods like oat
bran, beans, peas, and most fruits, is not digested by the body, but rather
fermented by bacteria in the colon, where it can cause gas. Insoluble fiber
is less likely to cause gas as it passes unchanged through the intestines and
30
DIET AND DISEASE
Table 1.21 Simple sugars that can cause gas

Simple carbohydrates that
cause gas
Dietary sources
Fructose
Also called fruit sugar
Found in onions, artichokes, pears, and wheat

May be added as a sweetener in some drinks
Lactose
Also called milk sugar
Found in milk products and processed foods that have

milk foods in them
Raffinose
Found in dried beans such as kidney, garbanzo, and

black beans
Found in lesser amounts in cabbage, Brussels sprouts,
broccoli, asparagus, and whole grains
Sorbitol
Sugar found in many fruits such as apples, pears,

peaches, and prunes
May be added as an artificial sweetener in diet and
sugar-free foods
is not fermented by colonic bacteria. Most fiber-containing foods have a

combination of soluble and insoluble fiber. Slowly increasing fiber intake
by a few grams per day and assuring adequate fluid intake alongside increasing fiber can help minimize gas associated with higher fiber intakes.
An additional precaution that can be taken to reduce gas is to reduce
the swallowing of air. Chewing foods slowly, avoiding drinking straws,
chewing gum, and assuring proper denture fit can all minimize the swallowing of air. For food-based gas reduction, advise those with gas to eat
small, frequent meals and to avoid high-fat fried foods and carbonated
beverages. Regular physical activity may also help alleviate gas. The use
of lactase enzyme supplements such as Lact-Aid may be useful in those
whose gas is caused by lactose intolerance.
Products such as Beano or Bean-zyme which provide alpha-galactosidase
can also be used. They reduce gas production by decreasing the amount
of undigested carbohydrate going into the large intestine. Table 1.22
contains a list of potentially gas-producing foods that may warrant ingestion of such an enzyme containing product before eating.
31
Table 1.22 Foods that may produce gas

Grains
Vegetables
Beans
Bagels
Beets
Black-eyed peas
Barley
Broccoli
Bog beans
Breakfast cereals
Brussels sprouts Broad beans
Granola
Cabbage
Chickpeas
Oat bran
Cauliflower
Lentils
Pasta
Corn
Lima beans
Rice bran
Cucumbers
Mung beans
Rye
Leeks
Peanuts and peanut butter
Sorghum
Lettuce
Pinto beans
Wheat bran
Onions
Red kidney beans
Whole wheat flour
Parsley
Seed flour (sesame, sunflower)
Whole grain breads Peppers, sweet
Soybeans and soy milk
Diarrhea
As is also the case with the previously mentioned GI maladies, diarrhea
is often a sign or symptom of another problem. Diarrhea affects nutritional status as it may cause rapid weight loss, dehydration, electrolyte
abnormalities, and acid-base imbalance, or it can also be indicative of a
malabsorptive disorder. Diarrhea is defined as the presence of loose,
watery stools passed at least three times per day. Diarrhea can also be
defined as >200 g/day stool weight passed by an adult. Acute diarrhea is
less than two weeks in duration, persistent diarrhea two to four weeks,
and chronic diarrhea lasts for more than four weeks (Camilleri and
Murray 2015).
Identifying the etiology and treating the underlying cause of diarrhea
is the primary goal of treatment. If infectious diarrhea is present, antibiotic therapy becomes the primary treatment. While the cause of diarrhea
can be attributed to many things, foods that may be related to diarrhea
include beans and legumes, high-fiber foods, high-fat foods, alcohol,
lactose, fructose, caffeine, and sorbitol (AND, 2015g). Clear liquids are
32
DIET AND DISEASE
not recommended for diarrhea because of their high osmolality, which

increases the likelihood of these foods drawing water into the lumen of
the intestine and further exacerbate diarrhea. Keeping a food and symptom diary may help identifying problem foods likely to trigger diarrhea.
Dietary management of diarrhea involves restoring normal fluid,
electrolyte, and acid-base balance. Other goals include slowing gut motility, thickening the consistency of the stool, repopulating the gut with
normal flora, and the eventual stimulation of the GI tract without exacerbating symptoms. Table 1.23 contains practical applications of these
dietary recommendations for the management of diarrhea.
Table 1.23 Dietary recommendations for managing diarrhea
(AND, 2015g)
Dietary recommendations for management of diarrhea
Restore Normal Fluid, Electrolyte, and Acid-Base Balance
Use oral rehydration solutions such as Pedialyte, Resol, Ricelyte, CeraLyte, and
Rehydralyte.
Decrease Gastrointestinal Motility
Avoid clear liquids and foods high in simple carbohydrates (lactose, sucrose or fructose).
Avoid sugar alcohols (sorbitol, xylitol, and mannitol).
Avoid caffeine.
Avoid alcohol.
Avoid high-fiber and gas-producing foods.
Thicken Consistency of Stool
Banana flakes, apple powder, or other pectin sources can be added to foods for adults.
Repopulate GI Tract with Normal Flora
Prebiotic and probiotic supplementation may help diarrhea, but current recommendations
do not include dosing information.
Stimulate GI tract by Introduction of Solid Food Without Exacerbating Symptoms
Choose low-fiber, low-fat, lactose-free foods initially.
Reintroduce lactose if no evidence of lactose intolerance.
33
Probiotics and Prebiotics for Diarrhea Treatment

Probiotic and prebiotic foods support the growth and repopulation of
healthy gut flora. As consumers increasingly look to dietary interventions
to help manage GI conditions, an emerging area of interest in the treatment of diarrhea involves the use of probiotic- and prebiotic-containing
foods. These agents are theorized to assist with diarrhea management by
either promoting water and electrolyte absorption in the colon and improving mucosal defense in the GI tract, or possibly reducing the growth
of harmful bacteria.
Probiotics are live microorganisms that facilitate good health in their
human hosts. Prebiotics are components in foods that good bacteria in the
large intestine use for fuel. Dietary sources of probiotics include yogurt or
dairy containing acidophilus, lactobacilli, and/or bifidobacteria, as well as
tempeh, miso, kim chi, or Kefir. The variety of strains of bacteria used in
different products alongside the difficulty inherent in maintaining the organisms viability has made it challenging to enact or recommend universal
dosing recommendations. However, recommending foods that contain
probiotics and prebiotics, such as yogurt, Kefir and cheese, is appropriate
(Douglas and Sanders 2008).
Celiac Disease
Celiac disease is an autoimmune disease also called gluten-sensitive enteropathy, or celiac sprue. In celiac disease, gluten (a protein found in
wheat, rye, and barley) ingested from the diet causes damage in the absorptive areas of the small intestine, resulting in villus atrophy. There is
no medication or surgical procedure that can reverse the effects of celiac
disease; in fact, the only therapeutic approach to managing celiac disease
is the maintenance of a gluten-free diet.
While estimations of the prevalence of celiac disease vary between
populations, higher rates are traditionally seen among Caucasians and
those of European descent. Prevalence rates of celiac disease in the United
States are thought to be 1:133 in the general population, and as high as
1:22 for those who have a first-degree relative (parent, sibling, or child)
who also has celiac disease (Fasano et al., 2003). Emerging evidence also
34
DIET AND DISEASE
supports the notion that individuals with other autoimmune conditions

(e.g., type 1 diabetes, Crohns disease) may also be at higher risk of developing celiac disease (Barera et al., 2002).
Symptoms of celiac disease vary widely and can range from general
irritable bowel complaints to constipation and diarrhea. Some people
are asymptomatic or have non-GI symptoms such as itchy skin or infertility. If a person has celiac disease and has been undiagnosed for a long
period of time, initial symptoms may be those of vitamin and mineral
deficiencies. Although biopsy of the small intestine remains the gold
standard in celiac disease diagnosis, people with celiac disease generally
have above average levels of particular antibodies. Testing for elevated
levels of anti-tissue transglutaminase antibodies (tTGA) or antiendomysium antibodies (EMA) can provide initial results pointing towards celiac disease. It is important to inform those suspecting celiac
disease that they should not intentionally avoid gluten-containing foods
before undergoing such antibody tests as false negatives will result with
exclusion of gluten in the period immediately preceding testing.
Nutritional Implications of Celiac Disease

In celiac disease, gluten damages and cuts down the villus height of the
small intestine. Because the small intestine is the primary site of nutrient
digestion and absorption, damage to its surface as a result of celiac disease
can result in profound nutrient deficiencies. Untreated celiac disease can
lead to deficiencies of iron, calcium, and folate, as these nutrients are
absorbed in the initial parts of the small intestine. Secondary lactose intolerance exists as a result of damage to the intestine, but tolerance may
improve alongside the gut healing that accompanies a gluten-free diet.
People with active lactose intolerance related to celiac disease are advised
to follow a lactose-reduced diet, with most needing a calcium supplement
with vitamin D to meet bone health needs.
Damage incurred further down the intestinal tract can cause carbohydrate malabsorption from secondary lactose intolerance, as well as
difficulties with absorption of fat and the fat-soluble vitamins A, D, E,
and K (S. Case 2010). Although absorbed in the proximal part of the
small intestine, vitamin B12 deficiency may be also be of concern in
35
celiac disease, particularly in cases of severe malabsorption (Case and

Kaplan 2003). Vitamin B12-rich foods are those of animal-origin: liver,
eggs, dairy, meat, poultry, and seafood. Supplementation of vitamin B12
may be indicated in those with low intakes of vitamin B12-containing
foods, and certainly for those following strict vegan diets that do not
contain animal foods.
The Gluten-Free Diet
The only therapy for celiac disease is dietary therapy and the maintenance
of a life-long gluten-free diet. Upon initial diagnosis of celiac disease,
many patients are overwhelmed by the perceived magnitude of dietary
changes that they are required to adopt for ultimate health. Focusing on
the foods that cant be a part of the diet quickly disheartens even the
most motivated newly diagnosed individual with gluten intolerance or
celiac disease. Rather, nutrition practitioners are encouraged to highlight
the variety of naturally occurring gluten-free foods that can be safely
included and enjoyed as a part of a well-balanced diet. While this does
involve initial education regarding gluten-containing and gluten-free
foods, with a little creativity and willingness to try new or not-so-familiar
grains and food items, most people with celiac disease can comfortably
adapt to the gluten-free realities of their nutrition requirements.
Because of the high-sugar, high-fat, high-calorie, and highcarbohydrate content of many packaged and prepared gluten-free foods
(such as cakes, cookies, breads, and crackers), people with celiac disease
should be cautioned that excessive intake of these foods will likely lead
to weight gain. A more nuanced and evolved approach to gluten-free
meal planning minimizes the use of gluten-free processed, packaged, and
prepared foods and instead emphasizes whole grains, fruits, vegetables,
low-fat or nonfat dairy, lean sources of protein, and naturally gluten-free
sources of carbohydrate. An excellent resource for motivated patients
trying to adopt a gluten-free diet is the book Gluten-Free Diet by
Canadian dietitian and celiac disease expert (and a person with celiac
disease herself) Shelley Case. Ms. Case has numerous resources and evidence-based guidelines about adhering to a gluten-free diet available on
her website at: https://www.glutenfreediet.ca.
36
DIET AND DISEASE
Diverticular Disease
In both the developed and developing parts of the world, rates of diverticular disease are rising alongside the increased reliance on and consumption of processed and packaged foods. Diverticular disease includes
diverticulosis (the presence of many small individual out-pouchings in
the colon called diverticulum), and diverticulitis (inflammation of the
diverticula that causes severe abdominal pain). Risk factors for the development of diverticulosis include having a history of constipation, low
fiber intake, high intakes of red meat, presence of obesity, and lack of physical activity (AND, 2015h). It is estimated that 10 percent of Americans ages
40 and older have diverticulosis and that one-quarter of those will develop
diverticulitis (Bogardus 2006).
From a dietary standpoint, fiber is the most important nutritional
component in the prevention of the development of diverticula, and
both soluble and insoluble fibers are involved here. Soluble fiber, which
absorbs water, adopts a soft, gel-like texture in the intestinal tract. Insoluble fiber, which is not absorbed, passes through the intestine unchanged and contributes to stool bulk. Manipulating both the texture
and bulk of the stools by increasing fiber in the diet helps to maintain
bowel regularity and prevents the development of diverticula (Tarleton
and DiBaise 2011).
While the importance of dietary fiber in the prevention of diverticular
disease cannot be overstated, it is important to note that the diet therapy for
the treatment of diverticulosis differs dramatically from that of diverticulitis.
With diverticulosis, the goal is to prevent the development of inflammation
and progression to diverticulitis. Diet therapy for diverticulosis includes a
high-fiber diet, with 6 to 10 grams of fiber per day encouraged above the
standard 20 to 35 gram recommendations. Recall that the average North
American eats only about 15 grams of fiber per day (ADA, 2008). A fiber
supplement consisting primarily of insoluble fiber may be helpful in meeting needs. In addition to assuring a high fiber intake, diverticulosis management may also be aided by the use of probiotic and prebiotic foods,
although again, current research does not substantiate recommended dosage
amounts (AND, 2015h). In the initial phase of diverticulitis, a nothing by
mouth diet order with bowel rest is advised until bleeding and diarrhea
37
resolve. The diet is then progressed to a clear liquid diet and may require
oral nutritional supplementation to help achieve optimal nutrition status. A
low-fiber therapy is initially recommended until the inflammation and
bleeding associated with diverticulitis are no longer a risk. After the acute
episode has resolved, dietary fiber intake should gradually be increased along
with water intake to the diverticulosis diet levels (6 to 10 grams above 20 to
35 gram recommendations). One recommended regimen is to advance the
diet by five grams of fiber per week until the goal is reached (Tarleton and
DiBaise 2011). Table 1.24 outlines the diet therapy recommendations for
the treatment of diverticulosis versus diverticulitis.
The Low Residue Diet in Diverticular Disease

Historically, clinicians would advocate a low-residue diet in the treatment of diverticulosis. As a review, residue refers to the indigestible matter of food that remains in the GI tract and contributes to the bulk of
stools. A low-residue diet restricts foods such as nuts, seeds, corn, and
popcorn under the premise that these items can enter, block, or irritate
an existing diverticulum and potentially cause diverticulitis. There is no
scientific evidence to support the recommendation of a low-residue diet,
which is also low in fiber, for the treatment of diverticulosis. In fact, the
opposite appears to be true: increasing dietary fiber can actually help reverse the pathophysiology of diverticular disease. The only justification
for recommendation of a low-fiber diet is during acute phase attacks of
diverticulitis. Table 1.25 contains a list of low-fiber foods to be initiated
with diet progression while resolving diverticulitis.
Table 1.24 Diet therapies for diverticulosis and diverticulitis

Diverticulosis diet therapy
Diverticulitis diet therapy
High-fiber diet of 610 g dietary fiber above NPO with bowel rest until bleeding and
standard 2035 g per day levels
diarrhea resolve
Consider use of a fiber supplement with
insoluble fiber to help meet needs
Advance to clear liquid diet
Probiotic foods (kefir, yogurt, miso) may be

helpful
Advance diet as tolerated, consider use of

supplements to meet nutrition needs
38
DIET AND DISEASE
Diverticulosis diet therapy
Diverticulitis diet therapy
No need to avoid nuts, seeds, corn, popcorn Initiate a low-fiber diet until inflammation
and bleeding no longer of concern
Increase fluid intake alongside increasing
fiber intake
When acute phase subsides, progress to highfiber, high-fluid diet

Probiotic foods may be helpful
Table 1.25 List of low-fiber foods for use in resolving diverticulitis

(AND, 2015h, AND, 2015h)
Low-fiber foods for use in resolving diverticulitis
Beef, poultry, fish
Milk
Bread, white
Nut butters, smooth
Cheese, all types
Pasta, white
Cottage cheese
Peaches, canned
Cream of wheat, instant
Pears, canned
Egg
Pudding or tapioca
Fruit juice
Rice, white
Green beans, canned
Soy, rice, or almond milk
Ice cream
Spinach
Lactose-free milk
Tofu
Lettuce
Tuna, canned
Mashed potatoes
Yogurt or soy yogurt
Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) refers to the group of disorders characterized by bloating, cramping, diarrhea, and constipation. IBS is a functional
bowel disorder (FBD) associated with bowel discomfort and abdominal
pains that occur alongside changes in bowel habits. IBS is diagnosed using
the Rome III criteria demonstrating at least three months, with onset at
least six months previously, of recurrent abdominal pain or discomfort,
associated with two or more of the following: improvement of pain with
defecation, onset associated with a change in frequency of stool, or onset
associated with a change in form (appearance) of stool. It is estimated that
39
IBS affects around 11 percent of the global population, of which only

about 30 percent who experience symptoms will consult a physician for
treatment (Canavan, West and Card 2014). The widely variable range of
symptoms and the highly individualized nature of the condition make it
one of the most frustrating GI disorders to either experience as a patient
or attempt to treat as a practitioner.
The causes of IBS are often debated but are still not entirely understood. Proposed theories for the underlying cause of IBS extend from
involvement of estrogen hormones in menstruating women to genetic
contributors, bacterial overgrowth, food allergies and food intolerances,
and infection or inflammation. Regardless of the cause of IBS, nutrition
practitioners should be sensitive to and aware of potential food-based
contributors and nutrition-related approaches to treatment. The nutrition assessment for IBS should identify any problems swallowing, the
presence of nausea or vomiting, constipation, diarrhea, heartburn, or
any other symptoms that interfere with normal food ingestion. Additional attention should be paid to high-fat foods, lactose, fructose, caffeine, sorbitol, and alcohol, which may exacerbate GI discomfort.
Thorough questioning of regular food, meal, alcohol, and other beverage intake patterns, and the use of 24-hour recall or food frequency questionnaire may help the practitioner identify offending or trigger foods or
beverages. Questioning the individual about supplement use or reliance on
laxatives or motility agents can also yield insightful information about the
IBS patients specific case. Encourage patients to keep a food and symptom
journal to track the types and quantities of foods consumed, along with GI
symptoms and emotional or life events that may trigger reactions. The
standard time frame for such journaling is usually three days, preferably
capturing two weekdays and one weekend day of food intake, GI symptoms, and emotional or other lifestyle contributors.
Once an understanding of the individuals IBS triggers and symptoms has been established, nutrition intervention involves normalizing
dietary patterns, eliminating culprit foods, gradually increasing dietary
fiber intake, utilizing bulking agents if needed, and considering the use
of prebiotics and probiotics (although current research does not substantiate dosage recommendations). Table 1.26 outlines considerations for
nutrition intervention in the individual with IBS.
40
DIET AND DISEASE
Table 1.26 Nutrition interventions for IBS

Nutrition Interventions for IBS
Normalize eating patterns
Discourage grazing; focus on small, frequent, low-fat meals and snacks at prescribed times
with well-balanced meal planning to assure adequacy of all nutrients.
Eliminate culprit foods
Identify food allergies and intolerances with special attention to fructose, caffeine, alcohol,
lactose, sorbitol, and raffinose (sugar found in beans, cabbage, Brussels sprouts, whole
grains, and other vegetables).
Keep a food diary
Track food intake, times of meals and snacks, quantities, and preparation methods as well
as related or associated GI symptoms and other emotional, environmental, or activityrelated contributors.
Increase fiber
Slowly increase fiber intake to 2535 g per day as tolerated with simultaneous increase of
fluid.
Try bulking agents
Bulking agents may improve constipation in certain individuals, although widespread
efficacy has not been recognized (Quartero et al., 2005).
Consider probiotics and prebiotics
Despite lack of universally agreed-upon dosing recommendations, the use of prebiotics and
probiotics, especially in yogurt, Kefir, and cheeses, may help in some IBS cases
FODMAPs Approach to IBS Management

One promising development for the dietary management of irritable bowel
syndrome and other functional gut disorders has been the implementation of
a low-FODMAPs diet. FODMAPs stands for Fermentable, Oligosaccharides, Disaccharides, Monosaccharides And Polyols, a group of short-chain
carbohydrates that are poorly absorbed by the human gut. These compounds
produce osmotic effects and have gas-producing capabilities that can set off
bowel-related symptoms. The human body does not have the enzyme required to break down oligosaccharides (including fructo-oligosacharides
(FOS) and inulin), resulting in their total inability to be absorbed. Polyols are
only partly absorbed, and absorption rates vary among individuals. Some,
41
but not all, individuals may also experience malabsorption with the presence
of fructose and lactose in the gut (Gibson 2011). It is important to note that
the presence of FODMAPs in the diet does not necessarily result in higher
rates of IBS-related symptoms, and FODMAPs are not the cause of functional bowel disorders. The approach to minimizing FODMAPs represents a
dietary approach to helping manage IBS symptoms, provided that all
FODMAPs, not just some, are addressed. Scientists at Monash University in
Australia originated the concept and have been leaders in the field with regards to publishing research regarding the effectiveness of the FODMAPs
approach.
The primary dietary sources of FODMAPs are found in foods with
fructose in excess of glucose, honey, apples and pears; fructans in wheat, rye,
onion, and garlic; galactans in cabbage and legumes; lactose in milk and
milk products; and polyols such as sorbitol and mannitol in stone fruits
(e.g., plums, cherries, mangos, peaches, apricots, and nectarines), mushrooms, and certain artificial sweeteners (Barrett and Gibson 2010). Referring candidates to a Registered Dietitian Nutritionist (RDN) trained in
developing a low-FODMAP diet may be an efficacious dietary approach to
minimizing IBS-related symptoms. The involvement of a specially trained
nutrition professional is essential as a low-FODMAP diet must be carefully
planned to meet patients individual needs and to identity any potential
nutrient deficiencies arising from eliminated foods and food groups.
Inflammatory Bowel Disease: Crohns Disease and Ulcerative Colitis

Inflammatory Bowel Disease (IBD) is an autoimmune disorder characterized by chronic inflammation of the gastrointestinal tract. IBD is a
syndrome that encompasses two distinct diseases: ulcerative colitis (UC)
and Crohns disease (CD). These two diseases are similar in nature but
distinguished from one another by their symptoms, GI involvement,
biopsy, and antibody testing. Global rates of IBD are highest in North
America, the United Kingdom, and Europe. Ashkenazi Jews have twice
the risk for IBD as do Israeli-born, Sephardic, or Oriental Jews. Ulcerative colitis and Crohns disease are most likely to afflict those aged 15 to
30 years, with a second peak occurring between 60 and 80 (Crohn's &
42
DIET AND DISEASE
Colitis Foundation of America 2011). Cigarette smoking doubles the

risk of Crohns but has a lesser effect on the development of UC.
With IBD, susceptible individuals experience inflammatory damages
in the GI tract that result in abdominal pain, diarrhea, and nausea and/or
vomiting. Ulcerative colitis afflicts the lower bowel, with particular involvement in the colon and rectum. Crohns disease is not characterized
by continuous inflammation, but instead the disease skips around the
GI tract and can affect any portion of the gut and bowel. Those with IBD
are at risk for developing conditions outside of the intestine as well, including osteopenia and osteoporosis, dermatitis, rheumatologic conditions, ocular symptoms, hepatobiliary complications, and kidney stones.
Complications of Crohns disease can include bowel obstruction, perforation and resection, fistulas, abscesses, and steatorrhea. In the most severe
cases, toxic megacolon and intestinal rupture can occur (AND, 2015i).
The presence of IBD dramatically increases nutrition risk. Between
60 to 75 percent of patients with Crohns are considered to be malnourished (Krok and Lichenstein 2003). In children with IBD, an increased
risk for insufficient bone mass and stunting exists. Table 1.27 outlines
the potential nutrient deficiencies and concerns for the person with IBD.
Table 1.27 Nutrition concerns in the person with IBD (AND, 2015i)
Nutrition concerns in the person with inflammatory bowel disease (IBD):
Nutrients
Deficiencies & concerns
Energy
Insufficient intake, loss of appetite, fear of abdominal pain following meals
Protein
Increased protein needs from GI losses caused by inflammation or

catabolism when infection or abscesses are present
Fluid &
Electrolytes
Short bowel syndrome may cause fluid losses
Iron
From blood loss, inadequate intake
Magnesium &
Zinc
Intestinal losses, particularly with short bowel syndrome
Calcium &
Vitamin D
Long-term steroid use & reduced intake of dairy foods with lactoserestricted diet
Vitamin B12
Surgical resection of stomach resulting in intrinsic factor loss or

resection of terminal ileum, the primary site of vitamin B12 absorption
Folate
Medications used to treat IBD may result in lower levels
43
Nutritional Management of IBD

The role of diet therapy in IBD management is to correct nutritional
deficiencies, reduce disease-related inflammation, and establish nutrient
adequacy in the diet. People with IBD often avoid foods or have particular food aversions that lead to insufficient nutrient intake. The use of
a food diary for people with IBD is helpful for practitioners attempting
to detect and identify nutritional inadequacies. When determining energy
needs, adult calorie levels are usually set at 25 to 35 kcal/kg, but this
may vary depending upon severity of disease, weight status, and nutritional deficiencies.
From a micronutrient standpoint, nutrition practitioners should use
the Dietary Reference Intake (DRI) levels as baseline recommendations,
while acknowledging that a person with IBD may need higher levels of
vitamins and minerals. The vitamins of particular concern include vitamin
B12, folate, thiamin, riboflavin, niacin, vitamin C, vitamin E, vitamin D,
and vitamin K. Minerals that may be needed in higher amounts include
iron (related to blood loss), zinc, magnesium, selenium, and potassium.
The use of omega-3 fatty acids, glutamine, and prebiotics may also be
helpful considerations in nutritional management of IBD (AND, 2015).
Nutrition intervention for active CD includes bowel rest with nutrition initially provided via total parenteral nutrition (TPN) or enteral
feedings. TPN is the preferred route of nutrition support in the presence
of fistulas; however, in other arenas, TPN has not been shown to be
more beneficial than enteral feedings for treating active IBD (AND,
2015i). For enteral nutrition, formulas that are elemental or peptidebased are preferred. Refeeding syndrome is common in IBD, and precautions to avoid refeeding should be taken into consideration when determining nutrition support or dietary regimens.
In the recovery period following exacerbations, the diet is slowly progressed to a low-fat, low-fiber, high-protein, high-calorie meal plan with
small, frequent meals. A low-fiber restriction is recommended only during acute flare-ups or in the presence of strictures (Eiden 2003). Previous
diet therapy recommendations for IBD included adherence to a lowresidue diet. Current recommendations do not include low-residue foods
or diets due to the lack of data demonstrating their efficacy. Vitamin or
44
DIET AND DISEASE
mineral supplements that may be required in active IBD and recovery

phases include vitamin D, zinc, calcium, magnesium, folate, vitamin
B12, and iron.
During remission, the nutritional goal is to maintain weight and to
replenish nutrient stores. Persons with IBD may find prebiotic and probiotic supplements to be helpful (Gassull, Ma and Pedrosa 2005);
furthermore, they may also benefit from omega-3 fatty acid and glutamine supplementation (Campos et al., 2003). Increasing antioxidant
intake (from food-based sources) and avoiding foods that are high in
oxalate are also recommended. Table 1.28 lists high-oxalate foods to be
avoided in IBD remission. Tables 1.29 and 1.30 contain lists of foods
recommended to include and to avoid with Crohns disease and ulcerative colitis.
Table 1.28 High-oxalate foods to avoid with IBD (AND, 2015)
High-oxalate foods to avoid with IBD
Drinks
Chocolate drink mixes, soy milk, Ovaltine, instant iced tea, fruit juices
of fruits from this table
Fruits
Dried apricots, red currants, figs, kiwi, rhubarb
Vegetables
Beans (wax, dried), beets and beet greens, chives, collard greens,
eggplant, escarole, dark greens of all kinds, kale, leeks, okra, parsley,
rutabagas, spinach, Swiss chard, tomato paste, watercress, zucchini
Breads, Cereals, Amaranth, barley, white corn flour, fried potatoes, fruitcake, grits,
and Grains
soybean products, sweet potatoes, wheat germ and bran, buckwheat
flour, All-Bran cereal, graham crackers, pretzels, whole wheat bread
Meat and
Proteins
Dried beans, peanut butter, soy burgers, miso
Desserts and
Sweets
Carob, chocolate, marmalades
Fats, Oils, Nuts, Nuts (peanuts, almonds, pecans, cashews, hazelnuts), nut butters, sesame
Seeds
seeds, tahini, poppy seeds
45
Table 1.29 Recommended foods for IBD (AND, 2015i)

Recommended foods for crohns
disease and ulcerative colitis
Notes
Dairy
Buttermilk
Evaporated, skim, powdered or low-fat milk
Smooth, nonfat or low-fat yogurt
Low-fat or reduced fat cheese
Low-fat ice cream or sherbet
Choose lactose-free products if lactose

intolerance present
Choose yogurt with live, active cultures-----see ingredient list on yogurt products
Proteins
Tender, well-cooked meats, poultry, fish,
eggs and soy prepared without added fat
Smooth nut butter
Grains
Bread, bagels, rolls, crackers, cereals, and
pasta made from white or refined flour
Choose grain foods with less than 2 g fiber

per serving
Vegetables
Most well-cooked vegetables without seeds
Potatoes without skin
Lettuce
Strained vegetable juice
Fruits
Fruit juice without pulp (except prune juice) Choose canned fruit in juice or light syrup
Ripe banana or melons
Most canned, soft fruits
Peeled apples
Fats and Oils
Limit to less than 8 tsp per day
Beverages
Water
Decaffeinated coffee
Caffeine-free tea
Soft drinks without caffeine
Very sweet juices or beverages with sugar or

high-fructose corn syrup may make diarrhea
worse in some people
46
DIET AND DISEASE
Table 1.30 Foods to avoid with IBD (AND, 2015i)

Foods to Avoid with Crohns Disease and Ulcerative Colitis
Dairy
Yogurt with berries, rinds, or nuts

Whole milk
Half and half, cream, sour cream
Ice cream (low-fat is OK)
Proteins
Fried meats, sausage, bacon

Luncheon meats such as bologna or salami
Hot dogs
Tough, chewy cuts of meat
Fried eggs
All dried peas, beans, and nuts
Chunky nut butters
Grains
Whole wheat or whole grain breads

Brown rice and wild rice
Cereals made from whole grain
Any grain food made with seeds or nuts
Vegetables
Beets
Broccoli
Brussels sprouts
Cabbage and sauerkraut
Cauliflower
Corn
Greens
Lima beans
Mushrooms
Okra
Onions
Parsnips
Peppers
Potato skins
Spinach
Squash
Fruits
All raw fruits except peeled apples, ripe bananas, or melons

Canned berries, canned cherries
Dried fruits, including raisins
Prune juice
Beverages
Beverages with caffeine: tea, cola, coffee, energy and sports drinks
Alcohol
Sweet fruit juices and soft drinks
Other
Sugar alcohols: sorbitol, mannitol, xylitol (found in sugar-free candy

and gum)
47
References
Academy of Nutrition and Dietetics. 2015. Xerostomia Treatment.
Nutrition Care Manual. http://www.nutritioncaremanual.org.
Accessed August 15, 2015.
.
___ 2015a. Dysphagia. Nutrition Care Manual. http://www.nutrition
caremanual.org. Accessed August 15, 2015.
___. 2015b. Gastroesophageal Reflux Disease. Nutrition Care Manual.
http://www.nutritioncaremanual.org. Accessed 2015, 15 August.
Accessed August 15, 2015.
___. 2015c. Peptic Ulcer Disease. Nutrition Care Manual. http://www
.nutritioncaremanual.org. Accessed August 15, 2015.
___. 2015d. Gastric Surgery. Nutrition Care Manual. http://www.
nutritioncaremanual.org. Accessed August 15, 2015.
___ 2015e. Constipation. Nutrition Care Manual. http://www.
nutritioncaremanual.org. Accessed August 15, 2015.
___. 2015f. Fluid Requirements. Nutrition Care Manual. http://www
.nutritioncaremanual.org. Accessed August 15, 2015.
___. 2015g. Diarrhea. Nutrition Care Manual. http://www.nutrition
caremanual.org. Accessed August 15, 2015..
___. 2015h. Diverticular Conditions. Nutrition Care Manual. http://
www.nutritioncaremanual.org. Accessed August 15, 2015.
___. 2015i. Inflammatory Bowel Disease. Nutrition Care Manual.
http://www.nutritioncaremanual.org. Accessed August 15, 2015.
___. 2015. Renal. Nutrition Care Manual. http://www.nutritioncare
manual.org. Accessed August 15, 2015.
Alaimo, K, et al. 1998. Dietary intake of vitamins, minerals, and fiber
of persons ages 2 months and over in the United States: Third
National Health and Nutrition Examination Survey, Phase 1, 19881991. Advance Data from Vital and Health Stastistics.
American Dietetic Association. 2010. International Dietetics and
Nutrition Terminology (IDNT) Reference Manual, 3rd ed. Chicago:
American Dietetic Association.
American Dietetic Association. 2008. Position Paper on Dietary
Fiber. Journal of the American Dietetic Association, 1716-1731.
48
DIET AND DISEASE
American Gastroenterological Association. 2013. Understanding

Constipation. http://www.gastro.org/patient-center/Understanding_
Constipation_Brochure_Jan_2013.pdf. Accessed September 15, 2015.
Atkinson, J, and A Wu. 1994. Salivary Gland Dysfunction: Causes,
Symptoms, Treatment. Journal of the American Dietetic Association.
125: 409-415.
Barak, N, ED Ehrenpreis, JR Harrison, and MD Sitrin. 2002. Gastrooesophageal Reflux Disease in Obesity: Pathyophysiological and
Therapeutic Considerations. Obesity Reviews. 3 : 9-15.
Barera, G, et al. 2002. "Occurrence of Celiac Disease After Onset of Type 1
Diabetes: A 6-Year Prospective Longitudinal Study." Pediatrics 109(5):
833-838.
Barrett, Jacqueline, and Peter Gibson. 2010. Development and
Validation of a Comprehensive Semi-Quantitative Food Frequency
Questionnaire that Includes FODMAP Intake and Glycemic
Index. Journal of the American Dietetic Association. 1469-1476.
Bogardus, ST Jr. 2006. What do We Know About Diverticular
Disease? A Brief Overview. Journal of Clinical Gastroenterology.
S108-111.
Bonnema, AL, LW Kolberg, W Thomas, and JL Slavin. 2010.
Gastrointestinal tolerance of chicory inulin products. Journal of
the American Dietetic Association. 110(6) : 865-868.
Camilleri, M, and JA Murray. 2015. Chapter 55. Diarrhea and
Constipation. In Harrison's Principles of Internal Medicine, by AS
Fauci, et al. New York: McGraw Hill.
Campos, FG, DL Waitzberg, MG Teixeira, DR Mucerino, DR Kiss,
and A Habr-Gama. 2003. Pharmacological Nutrition in
Inflammatory Bowel Diseases. Nutricin Hospitalaria. : 57-64.
Canavan, C, J West, and T Card. 2014. "The epidemiology of irritable
bowel syndrome." Clin Epidemiol. 6 : 71-80.
Case, S, and CR Kaplan. 2003. Gluten-Free Guidance: Practical Tips
for Dietitians and their Celiac Patients. Today's Dietitian,3: 44-49.
Case, Shelley. 2010. Gluten-Free Diet: A Comprehensive Resource
Guide. Regina, Saskatchewan: Case Nutrition Consulting, Inc.
49
Chey, WD, and BC Wong. 2007. American College of Gastroenterology

Guideline on the Management of Helicobacter Pylori Infection.
American Journal of Gastroenterology. 102(8): 1808-1825.
Crohn's & Colitis Foundation of America. 2011. Facts About
Inflammatory Bowel Disease. http://www.ccfa.org/resources/factsabout-inflammatory.html Accessed September 15, 2015.
Douglas, LC, and ME Sanders. 2008. Probiotics and Prebiotics in
Dietetics Practice. Journal of the American DIetetic Association.:
510-521.
Duro, D, and C Duggan. 2007. The BRAT Diet for Acute Diarhea.
Practical Gastroenterology. : 60-68.
Eiden, K. Nutritional Considerations in Inflammatory Bowel Disease.
2003. Practical Gastroenterology.: 33-50.
Eisbruch, A. 2007. Reducing Xerostomia by IMRT: What May, and
May Not, be Achieved. Journal of Clinical Oncology 25 (31):
4863-4864.
Falk, GW, and DA Katzka. 2012. "Diseases of the esophagus." In
Goldman's Cecil Medicine, by L Goldman and AI Schafer, 203213. Philadelphia, PA: WB Saunders.
Fasano, A, et al. 2003. Prevalence of Celiac Disease in At-RIsk and
Not-at-risk Groups in the United States: A Large Multicenter
Study. Archives of Internal Medicine 10,163(3): 286-292.
Gassull, MA, J Ma, and E Pedrosa. 2005. Macronutrients and
Bioactive Molecules: Is There a Specific Role in the Management of
Inflammatory Bowel Disease. Journal of Parenteral and Enteral
Nutrition. : S179-182.
Gibson, P. 2011. Food intolerance in functional bowel disorders.
Journal of Gastroenterology and Hepatology.: 128-131.
Hasler, WL. 2015. Nausea, Vomiting and Indigestion. Harrison's
Principles of Internal Medicine. 19e. New York, NY: McGraw Hill.
Institute of Medicine. 2005. Dietary Reference Intakes for Energy,
Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and
Amino Acids. Washington, DC: National Academies Press.
King, DE, AG 3rd Mainouse, and CA Lambourne. 2012. "Trends in
dietary fiber intake in the United States, 1999-2008." Journal of the
Academy Nutrition Dietetics. 112(5): 642-648.
50
DIET AND DISEASE
Krok, KL, and GR Lichenstein. 2003. Nutrition in Crohn's Disease.

Gastroenterology, : 148-153.
Mahan, LK, and S Escott-Stump. 2008. Krause's Food & Nutrition
Therapy. 12th ed.. St. Louis, MO: Saunders Elsevier.
Makola, D, DA Peura, and SE Crowe. 2007. Helicobacter Pyrlori
Infection and Related Gastrointestinal Diseases (Review). Journal
of Clinical Gastroenterology. 41(6) : 548-558.
Marlett, J, and TF. Cheung. 1997. Database and Quick Methods of
Assessing Typical Dietary Fiber Intakes Using Data for 228
Commonly Consumed Foods. Journal of the American Dietetic
Association. 1139-1151.
McCallum, SL. 2003. The National Dysphagia Diet: Implementation
at a Regional Rehabilitation Center and Hospital System. Journal
of the American Dietetic Association. 103 (3) : 381-384.
McCullough, G, C Pelletier, and C Steele. 2003. National Dysphagia
Diet: What to Swallow? The ASHA Leader.
National Digestive Diseases Information Clearing House. Digestive
Diseases. 2013. http://digestive.niddk.nih.gov/ddiseases/pubs/gas/.
Accessed August 15, 2015..
National Institute of Diabetes and Digestive and Kidney Diseases.
Digestive Disease Statistics for the United States. 2014. http://
www.niddk.nih.gov
/health-information/health-statistics/Pages/digestive-diseases-statisticsfor-the-united-states.aspx. Accessed September 15, 2015.
Nelms, Marcia. 2011. Disease of the Upper Intestinal Tract. In
Nutrition Therapy & Pathophysiology, by Marcia Nelms, Kathryn
Sucher, Karen Lacey and Sara Long Roth, 352. Belmont, CA:
Wadsworth.
Nelms, Marcia. 2011. Diseases of the Lower Intestinal Tract. In
Nutrition Therapy & Pathophysiology, by Marcia Nelms, Kathryn
Sucher, Karen Lacey and Sara Long Roth, 424. Belmont, CA:
Wadsworth.
O'Connell, MB, DM Madden, AM Murray, RP Heaney, and LJ
Kerzner. 2005. Effects of Proton Pump Inhibitors on Calcium
Carbonate Absorption in Women; A Randomized Control Trial.
American Journal of Medicine. 117(7): 778-781.
51
O'Donnell, K. 2008. Small but Mighty: Selected Micronutrient Issues

in Gastric Bypass Patients. Practical Gastroenterology. 32(5): 37-48.
Quartero, AO, V Meineche-Schmidt, J Muris, G Rubin, and N de Wit.
2005. Bulking agents, antispasmodic and antidepressant medication
for the treatment of irritable bowel syndrome. Cochrane Database
Systemic Reviews: CD003460.
Schafer, TF. 2012. Peptic Ulcer Disease.. http://www.acg.gi.org/patients
/gihealth/peptic.asp. Accessed August 15, 2015.
Schiller, LR. 2008. Nutrients and Constipation: Cause or Cure?
Practical Gastroenteroly. : 43-49.
Shepherd, SJ, FC Parker, JG Muir, and PR Gibson. 2008. Dietary
triggers of abdominal symptoms in patients with irritable bowel
syndrome: randomized placebo-controlled evidence. Clinical
Gastroenterology and Hepatology.
Stewart, ML, SD Nikhanj, DA Timm, W Thomas, and JL Slavin.
2010. Evaluation of the effect of four fibers on laxation,
gastrointestinal tolerance and serum markers in healthy humans.
Ann Nutr Metab. 56(2): 91-8.
Storey, D, A Lee, F Bornet, and F Brouns. 2007. Gastrointestinal
responses following acute and medium term intake of retrograded
resistant maltodextrins, classified as type 3 resistant starch.
European Journal of Clininical Nutrition. 61(11) : 1262-70.
Tan, KY, and F. Seow-Choen. 2007 Fiber and Colorectal Diseases:
Separating Fact from Fiction. World Journal of Gastroenterology. :
4161-4167.
Tarleton, Sherry, and John K DiBaise. 2011. Low-Residue Diet in
Diverticular Disease: Putting an End to a Myth. Nutrition in
Clinical Practice.: 137-142.
Wardlaw, GM, and AM Smith. 2011. Contemporary Nutrition. 8th ed.
New York, NY: McGraw Hill.
Yang, YX, JD Lewis, S Epstein, and DC Metz. 2006. Long-Term
Proton Pump Inhibitor Therapy and Risk of Hip Fracture. Journal
of the American Medical Association 296. : 2947-2953.
Index
Academy of Nutrition and Dietetics,
27, 70, 93, 100, 101
Acute diarrhea, 31
Acute hepatitis, 95
Alcohol abuse, chronic
cirrhosis and, 94
nutrition supplements
recommended for, 94t
Alcohol, gout and, 71
American Academy of Pediatrics, 64
American Gastroenterological
Association, 24
American Liver Foundation, 91
Anemia, 7685
iron deficiency, 7681
megaloblastic, 8184
pernicious, 8182
sickle cell, 8485
Animal protein, role of, 65
Antibiotic therapy, PUD and, 15
Antiendomysium antibodies (EMA), 34
Anti-tissue transglutaminase
antibodies (tTGA), 34
Aspiration, GERD and, 13
Aspirin, peptic ulcer disease and, 15
Atrophic gastritis, 82
Beano, 30
Bean-zyme, 30
Bone density
dual energy x-ray absorptiometry
for, 56
guide for understanding T-scores, 57t
test for, 57
Bone loss, animal protein and, 65
Bone mineral density (BMD), 56
Calcium
for chronic kidney disease, 100
dairy foods and content, 59t
on dialysis, 100
dietary reference intakes:
recommended dietary
allowances for, 58t
intake and recommendations for
weakened bones, 5861
non-dairy foods and content, 60t
practical method for estimating
individual daily intake, 61t
recommendations for
postmenopausal women and
men aged 50 and older, 6667
supplements, 6162, 62t
Calcium acetate, 107
Calcium carbonate, 62, 62t, 107
Calcium citrate, 62, 62t, 107
Calcium oxalate, 98
Calcium phosphate, 98
Calories
on dialysis, 100
Celecoxib, 68
Celiac disease, 3334, 82
for dietary therapy, 35
estimations of prevalence of, 33
gluten-free diet, 35
nutritional implications of, 3435
prevalence rates of, 33
symptoms of, 34
Celiac sprue. See Celiac disease
Children
iron deficiency in, 76
with sickle cell disease, 84
Chondroitin, for osteoarthritis, 6869
Chronic diarrhea, 31
Chronic kidney disease (CKD), 98107
characterization of, 98
definition of, 98
goal of management of
phosphorus, 104
112
INDEX
Chronic kidney disease (Continued )

high-phosphorus foods to limit or
avoid in, 105106t
non-dialysis, 99
nutrition prescription for, 100
nutrition therapies for
management of, 98
phosphorus, 104107
potassium, 101104
stages of, 99t
Chylomicrons, 6
Cirrhosis, 9294
caused by, 92
foods to avoid, 93
nutritional management for, 93
nutrition therapy for, 93
Clinicians Guide to Prevention and
Treatment of Osteoporosis, 65
Constipation, 2429
causes of, 24
definition of, 24
dietary fiber and, 2426
fluid intake and, 2728, 28t
functional fibers, 2627
medication inducing, 24
physical activity and additional
approaches to combatting, 29
possible nutrition diagnosis related
to, 24t
Corticosteroids, peptic ulcer disease
and, 15
Crohns disease (CD), 4144, 82
complications of, 42
foods to avoid with, 46t
nutrition intervention for, 43
recommended foods for, 45t
Diabetes, fatty liver and, 92
Dialysis, micronutrient regimen for,
101t
Diarrhea, 3133
definition of, 31
dietary management of, 32, 32t
etiology and treating underlying

cause of, 3132
probiotics and prebiotics for
treatment, 33
Dietary fiber
adequate intake recommendations
for, 25t
constipation and, 2426
determining from food records, 26t
functional fibers, constipation and,
2627
gas and, 29
importance of, 36
tips for increasing intake, 27t
Dietary interventions, bone loss and, 57
Dietary Reference Intake (DRI), 25,
43, 58
Diet, low residue, 3738
Diet therapy
for celiac disease, 35
for diverticulosis and diverticulitis,
3738t, 3839t
for gallstones, 97
gastroesophageal reflux disease, 14t
in inflammatory bowel disease, 43
for peptic ulcer disease, 17
for rheumatoid arthritis, 71t
Digestive disorders, 1
Digestive system, healthy, nutrition
and, 1
Diverticular disease, 3637. See also
Diverticulosis; Diverticulitis
low residue diet in, 3738
Diverticulitis
diet therapies for, 3738t, 3839t
initial phase of, 3637
low-fiber foods for use in resolving,
39t
risk factors for development of, 36
Diverticulosis, diet therapies for, 36,
3738t, 3839t
Docosahexaenoic acid (DHA), 76
Dry mouth, 89, 75
INDEX
Dual energy x-ray absorptiometry

(DEXA), for bone density, 56
Dumping syndrome, 1920
management of, 19
results in, 19
symptoms of, 19
Duodenum, 2, 5
Dysphagia, 912, 75. See also specific
dysphagias
complications of, 10t
definition of, 9
National Dysphagia Diet
food considerations, 11t
liquid consistencies, 12t
nutritional consequences of
untreated, 10t
nutritional management of, 1012
Eicosapentaenoic acid (EPA), 76
Enteral nutrition, 43
Esophageal dysphagia, 9
Estrogen, bone health and, 5455
Fatty liver, 92
causes of, 92
symptoms of, 92
treatment for, 92
Fermentable, Oligosaccharides,
Disaccharides,
Monosaccharides And
Polyols (FODMAPs)
approach to IBS management, 4041
primary dietary sources of, 41
Fibers
dietary, 2426
functional, 2627
insoluble
in fruits and vegetables, 25
gas and, 29
soluble and insoluble, 36
Fibromyalgia, 74
Fluid intake
for gallstones, 97
kidney stones and, 98
113
Fluid restriction, for chronic kidney

disease, 100
Folate
megaloblastic anemia by
deficiency, 8384
RDA for, 84
Folic acid, 83
tolerable upper intake level (UL)
for, 8283
vitamin B12 and, 82
Food diary, use for inflammatory
bowel disease, 43
Food-first approach, 61
Fructo-oligosacharides (FOS), 40
Fructose, 30t
Functional bowel disorder (FBD), 38
Gallstones, 97
Gastric acid, in esophagus, 13
Gastric surgery, 1820
dietary interventions in postsurgery, 20t
dumping syndrome, 1920
foods to avoid after, 2223t
foods to include after, 21t
potential micronutrient
deficiencies following, 20t
procedures, 18t
Gastroesophageal reflux disease
(GERD), 1214
diet therapy for, 14t
hiatal hernia and, 1415
nutrition interventions and goals
in, 14t
Gastrointestinal (GI) tract
lower, medical nutrition therapy
for disorders of, 2346
upper, medical nutrition therapy
for disorders of, 823
Glucosamine/chondroitin Arthritis
Intervention Trial (GAIT), 68
Glucosamine, for osteoarthritis,
6869
114
INDEX
Glutamine, 43, 44
Gluten-free diet, 35
Gluten-sensitive enteropathy. See
Celiac disease
Gout, 7174
low, moderately high and very high
purine foods, 7273t
nutrition interview considerations
for the individual with, 72t
nutrition recommendations for
acute attacks and between
gouty flare-ups, 7374t
risk of, 71
Gouty flare-ups, 71
Helicobacter pylori, 15
Heme iron, 78
Hemochromatosis, 81
Hemodialysis (HD), 99
potassium needs and restrictions
in, 101
Hemoglobin, 80
Hepatitis, 95
Hiatal hernia, 1415
GERD and, 14
High-density lipoproteins (HDLs),
7, 7t
Hip fracture, 54
Hydrochloric acid (HCl), 18
Hyperkalemia, 101
Ileocecal sphincter, 3
Ileum, 2, 5
Infectious diarrhea, 31
Inflammatory bowel disease (IBD),
4144. See also Crohns
disease; Ulcerative colitis
diet therapy in, 43
food diary for, 43
global rates of, 41
high-oxalate foods to avoid with, 44t
nutrition concerns in person with, 42t
presence of, 42
Insoluble fiber
in fruits and vegetables, 25
gas and, 29
Institute of Medicines Food and
Nutrition Board, 58
Institutes of Medicine (IOM), 64
Intestinal gas, 2931
foods producing, 31t
precautions for reducing, 30
simple sugars causing, 30t
Intrinsic factor, pernicious anemia
and, 8182
Iron, 7681
absorption, 78
approaches to enhancing, 79t
factors limiting, 78t
childhood poisoning and toxicity,
81
containing foods, 79t
dietary sources of, 78
factors increasing risk of deficiency,
77
recommended dietary allowances
for, 77t
supplements, 7981
tolerable upper intake level for, 81
Irritable bowel syndrome (IBS),
3841
causes of, 39
FODMAPs approach to
management, 4041
nutrition assessment for, 39
nutrition interventions for, 40t
triggers and symptoms, 39
Jejunum, 2, 5
Kidney stones, 9798
nutrition prescription for, 98
types of, 97
Kyphosis, 54
INDEX
Lact-Aid, 30
Lactose, 30t
Large intestine, 2
Lipid absorption, 6
Lipoproteins, 7, 7t
Low-density lipoproteins (LDLs), 7, 7t
Lower esophageal sphincter (LES), 3,
1213
Low-fiber therapy, 37
Low residue diet, diverticular disease,
3738t
Lupus, 7576
causes of, 75
diet and, 75
Lupus Foundation of America, 75
Mannitol, 41
Medical nutrition therapy
for gout, 72
of lower GI tract, 2346
Megaloblastic anemia
by folate deficiency, 8384
by vitamin B12 deficiency, 8283
Metabolic syndrome, fatty liver and, 92
Microvilli, 23
Minerals, in IBD management, 4344
Muscular sphincters, digestion and, 3
National Center for Complementary
and Alternative Medicine
(NCCAM), 68
National Dysphagia Diet (NDD), 10
food considerations, 11t
liquid consistencies, 12t
National Health and Nutrition
Examination Survey
(NHANES), 62
National Institute of Arthritis and
Musculoskeletal and Skin
Diseases (NIAMS), 68
National Institute of Diabetes and
Digestive and Kidney
Diseases, 91
National Institutes of Health (NIH), 68
115
National Kidney Disease Education

Program (NKDEP), 104
National Kidney Foundation, 97, 98
The National Osteoporosis
Foundation, 53, 54
Nephrolithiasis. See Kidney stones
Non-heme iron, 78
Nonsteroidal, anti-inflammatory
drugs (NSAIDs), 15
Nothing by mouth diet order, 37
Nutrient
absorption, 46, 56t
digestion of, 24
transport of, 67
Obesity
fatty liver and, 92
and osteoarthritis, 68
Omega-3 fatty acids, 43, 44
Oropharyngeal dysphagia, 9
Osmosis, 5
Osteoarthritis (OA), 6768
glucosamine and chondroitin use
for, 6869
overweight and obesity, 68
Osteomalacia, 63
Osteoporosis
causes, 53
conditions that increasing, 56t
diagnosing, 5657
risk factors for, 5456, 5556t
significance of, 54
Overweight, and osteoarthritis, 68
Oxalates, 78, 78t
Pancreatic enzyme supplementation,
use of, 96
Pancreatitis, 9596
caused by, 95
nutrition therapy goal, 96
pain control and intravenous
hydration, 96
vitamin supplementation for, 96
116
INDEX
Peptic ulcer disease (PUD), 1517

abdominal discomfort with, 16
diet therapy for, 17
factors exacerbating, 16t
foods not recommended for, 17t
medication and nutritional
management of, 1517
non-medication-related
management of, 15
Pepto-Bismol, 15
Peritoneal dialysis (PD), 99
potassium needs and restrictions
in, 101
Pernicious anemia, 8182
Phosphate binders, 107
Phosphorus, 104107
goal of CKD management of, 104
high-phosphorus foods, 105t
lower phosphorus alternatives for
high-phosphorus foods, 106t
Phytates, 78, 78t
Potassium, 101104
on dialysis, 100
high-potassium foods, 102t
leaching from vegetables, 104t
low-potassium foods, 103t
Prebiotics, 43
for diarrhea, 33
Pregnancy
folate in, 83
GERD during, 13
RDA increase, 84
Probiotics, for diarrhea, 33
Protein
for bone health, 65
on dialysis, 100
hepatitis and, 95
intake for gallstones, 97
Protein-calorie malnutrition (PCM), 98
Proton pump inhibitor (PPI), PUD

and, 15
Purine foods, gout and, 72
Pyloric sphincter, 3
Raffinose, 30t
Recommended Dietary Allowance
(RDA), 58
Refeeding syndrome, 43
Registered Dietitian Nutritionist
(RDN), 41
Rheumatic disease, 6675
fibromyalgia, 74
gout, 7174
osteoarthritis, 6768
glucosamine and chondroitin use
for, 6869
rheumatoid arthritis, 6971
Sjogrens syndrome, 75
Rheumatoid arthritis (RA), 6971
diet therapy for, 71t
nutritional status in person with, 69
nutrition interview questions for, 70t
Rickets, 63
Saliva, 8
Secondary lactose intolerance, 34
Serum 25-hydroxyvitamin D
(25(OH)D), 64
Sickle cell disease (SCD), 8485
calories and protein for, 84
causes, 84
maintaining adequate fluid status
in, 85
micronutrient deficiencies in, 84
nutrition recommendations for, 84
Sippy diet, 17
Sjogrens syndrome, 75
Small intestine
biopsy of, 34
nutrient digestion and absorption,
4, 34
INDEX
Smoking, Crohns disease and, 42

Sodium
for bone health, 65
on dialysis, 100
Soluble fiber, gas and, 29
Sorbitol, 30t, 41
Spina bifida, 83
Struvite, 98
Supplemental iron, 7981
Swallowing, proper, 9
Systemic lupus erythematosus (SLE).
See Lupus
Tannins, 78, 78t
Tolerable Upper Intake Level (UL),
for calcium, 62
Total parenteral nutrition (TPN), 43
T-score reading, osteoporosis and, 57
Ulcerative colitis, 4144
Uric acid, cysteine, 98
Urinary tract stone disease. See
Kidney stones
Urolithiasis, 97
117
Vertebrae, osteoporosis-related
fractures of, 54
Very low-density lipoproteins
(VLDLs), 7, 7t
Vitamin B12, 3435
and folic acid, 82
megaloblastic anemia by
deficiency, 8283
pernicious anemia and, 8182
treatment for deficiency, 83
Vitamin C, iron and, 78, 80
Vitamin D
content of various foods, 63, 63t
dietary reference intakes for, 64t
intake and recommendations for
weakened bones, 6364
roles of, 63
supplements, 6465
Vitamins, in IBD management, 4344
Weight-bearing exercises, bone loss
and, 57
Xerostomia. See Dry mouth
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Diet and Disease

Diet and Disease

Diet and Disease: Nutrition for Gastrointestinal, Musculoskeletal, Hepatobiliary,

Nutrition and Gastrointestinal Disorders ..........................1

Primary sites of nutrient absorption ..................................5

Lipoproteins, their content, roles in the body and

Xerostomia treatment techniques and

Nutritional consequences of untreated

The National Dysphagia Diet food considerations

National Dysphagia Diet liquid consistencies

Nutrition interventions and goals in patients with

Diet therapy for patients with GERD (AND, 2015b),

Factors that exacerbate peptic ulcer disease

Table 1.10 Foods not recommended for people with peptic

Table 1.17 Dietary reference intake adequate intake

Osteoporosis risk factors (NOF, 2015c),

Conditions that increase osteoporosis risk

WHO DEXA T-Score result diagnostic criteria

Dietary reference intakes: recommended dietary

Dairy foods and calcium content (Nelms 2011),

Nondairy foods and calcium content (Nelms 2011),

Practical method for estimating individual

Calcium supplements .....................................................62

Vitamin D content of various foods

Table 2.10 Dietary reference intakes for vitamin D

Nutrition supplements recommended for chronic

Five stages of chronic kidney disease (NKF, 2015a) ........99

Micronutrient regimen for individuals on dialysis

High-potassium foods to limit to no more than 1

Low-potassium foods that are appropriate in

How to leach potassium from high-potassium

How to leach potassium from high-potassium

High-phosphorus foods to limit or avoid in CKD

Lower phosphorus alternatives for high-phosphorus

DIET AND DISEASE

to the basics of nutrient digestion, absorption, and transport and then

Nutrient Digestion, Absorption, and Transport

Carbohydrate digestion involves the breakdown of complex

NUTRITION AND GASTROINTESTINAL DISORDERS

From a chemical standpoint, digestive juices, or enzymes, are secreted

Lower esophageal sphincter: located between the bottom of

Digestion begins in the mouth, where salivary amylase secreted from

DIET AND DISEASE

NUTRITION AND GASTROINTESTINAL DISORDERS

protein; absorption of the simple sugar fructose is enabled by facilitated

Primary nutrients absorbed

Minerals: calcium, phosphorus, magnesium, iron, zinc, chromium,

DIET AND DISEASE

Primary nutrients absorbed

NUTRITION AND GASTROINTESTINAL DISORDERS

The liver produces lipoproteins of varying densities. Very low-density

and TG from liver to

What is left after cells

Large, light, and

DIET AND DISEASE

Medical Nutrition Therapy for Disorders

NUTRITION AND GASTROINTESTINAL DISORDERS

DIET AND DISEASE

Table 1.4 Nutritional consequences of untreated dysphagia

Nutritional Management of Dysphagia

NUTRITION AND GASTROINTESTINAL DISORDERS

Table 1.5 The National Dysphagia Diet food considerations

Smooth, pureed, homogenous, cohesive foods of pudding-like consistency